As the core regulatory hub of cellular metabolism and life activities, mitochondria play a crucial role in energy metabolism, the balance of oxidative stress, and the determination of cell fate. Their dysfunction is closely associated with the pathological progression of major diseases such as neurodegenerative diseases, cardiovascular diseases, and metabolic syndromes. Mitochondrial transplantation technology provides a novel strategy for repairing cellular metabolic damage and reversing pathological states by exogenously supplementing functional mitochondria, and has attracted widespread attention in the fields of cell therapy and regenerative medicine in recent years. Although this technology has demonstrated significant potential in basic research and early clinical exploration, it still faces numerous challenges in terms of technical optimization, ethical norms, and clinical translation. This article systematically reviews the cutting-edge progress of mitochondrial transplantation technology, and comprehensively analyzes the core elements including the screening of mitochondrial donor cells, isolation and purification processes, construction of efficient delivery systems, and efficacy evaluation methods. It also deeply explores the application prospects and mechanisms of mitochondrial transplantation in multiple fields, such as neurodegenerative disease repair, cardiovascular function remodeling, metabolic disease intervention, novel tumor treatment strategies, reproductive health protection, and aging delay. Moreover, it analyzes the technical bottlenecks and ethical controversies in current research, and looks forward to future development directions, aiming to provide theoretical references and practical guidance for in-depth research and clinical translation in this field.
Many proteins are closely associated with the onset and progression of diseases, making them key targets for clinical diagnosis and treatment prognosis. However, the detection of target proteins presents significant challenges due to their low expression in the early stages of disease, limited recognition elements, and susceptibility to inactivation. Aptamers, a promising class of short single-stranded oligonucleotides, exhibit high affinity and specificity for recognition. They are widely used in protein detection and analysis due to their small size, modifiability, high selectivity, and stability. Meanwhile, the Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated proteins system (Cas) system, known for its unique and efficient trans-cleavage amplification effect, has become a vital technology in the field of biosensing in recent years. The combination of aptamers and the CRISPR/Cas system have the potential to fully harness their strengths in protein recognition and signal amplification, enabling highly sensitive and specific detection of low-abundance proteins, thereby offering robust technical support for early disease diagnosis. This review categorizes and evaluates recent advancements in protein detection using aptamers combined with the CRISPR/Cas system. It primarily introduces the working principles of aptamers and the CRISPR/Cas system, as well as the combination of these two biosensor techniques. Then, we summarize and analyze research advancements and application strategies for protein detection technologies that leverage the synergistic effects of both methods in biosensing platforms, including colorimetry, fluorescence, and electrochemistry. We also encompass the integrated application of novel detection methods such as the enhancement by nanomaterials (e.g., gold nanoparticles, metal-organic frameworks, MXene, etc.), resonance Rayleigh scattering (RRS), and surface-enhanced Raman scattering (SERS). Finally, we discuss the current challenges facing this area of research and explores potential counterstrategies. In sum, we provide a forward-looking perspective on this technological field, aiming to serve as a systematic reference for technical innovation and clinical translation, thereby laying the groundwork for future research in precise and sensitive protein detection
Retinitis pigmentosa (RP), Leber’s congenital amaurosis (LCA), and age-related macular degeneration (AMD) are three representative inherited ocular diseases. Traditional treatments, such as nutritional support and anti-VEGF drugs (for wet AMD), can partially delay disease progression but are limited by incomplete efficacy, complex treatment regimens, and potential drug resistance with long-term use. In recent years, the rapid development of clustered regularly interspaced short palindromic repeats (CRISPR) and CRISPR-associated (Cas) protein systems have opened new avenues for the definitive treatment of inherited ocular diseases. The CRISPR-Cas9 system and its derived tools enable direct correction of pathogenic gene mutations in the retina, demonstrating great therapeutic potential for inherited ocular disorders. This review summarizes the latest research advances in CRISPR-Cas9, base editors, and prime editors for inherited ocular diseases such as RP, LCA, and AMD. We focus on the disease-specific mechanisms of gene editing therapies and the challenges faced during clinical translation, providing theoretical support to accelerate the clinical application of CRISPR-based gene editing in inherited ocular diseases.
Transient receptor potential vanilloid (TRPV) channels, as non-selective cation channels, play a central role in various physiological and pathological processes, and their dysregulation has been strongly associated with skin cutaneous melanoma (SKCM). This review systematically summarizes the research progress on the expression regulation, molecular mechanisms, tumor microenvironment roles, and therapeutic resistance of TRPV1, TRPV2, and TRPV4 in SKCM. Notably, TRPV family members exhibit functional divergence and context-dependency in SKCM: TRPV1 exerts a tumor-suppressive function by inducing apoptosis via calcium influx, whereas TRPV2 and TRPV4 promote melanoma invasion and metastasis by regulating calcium signaling, Akt pathway, and cytoskeletal remodeling. Upregulation of TRPV2 is associated with interactions within the tumor microenvironment (TME), and TRPV4 can either drive metastasis or induce ferroptosis depending on the activation intensity, highlighting the complexity and controversy of this family's functions. Moreover, TRPVs modulate immune checkpoint molecules(e.g., PD-L1) and drug resistance pathways(e.g., PI3K/Akt), thereby facilitating immune evasion and chemoresistance. Despite the therapeutic promise of TRPVs agonists and antagonists, challenges in subtype selectivity and clinical translation persist as obstacles. This review systematically delineates the functional divergence and complexity of TRPV channels in skin cutaneous melanoma, highlights the major challenges currently facing targeted therapy against this family, and provides a theoretical basis and strategic outlook for TRPVs-targeted therapy in skin cutaneous melanoma.
Proline hydroxylase domain (PHD) is an oxygen-sensing protein of the dioxygenase family. It can regulate the activity of hypoxia-inducible factor (HIF) and the expression of related genes by sensing changes in partial pressure of the oxygen. Currently, four types of PHDs have been discovered in mammalian cells, including PHD1, PHD2, PHD3, and prolyl 4-hydroxylase possessing a transmembrane domain (P4H-TM). Among them, PHD2 is the key enzyme for degradation of the HIF α subunit. A lot of research has confirmed that the change of PHD2 activity is the initial step in the hypoxic response induced by tumor cells. Besides oxygen pressure, other factors include binding of the substrate 2-oxoglutarate (2OG) or cofactors Fe2+and ascorbic acid, or the chemical modification and interaction with regulatory proteins. All of these can affect the activity of PHD2 and its multiple regulatory functions. Abnormal expression of PHD2 has been detected in malignant tumors. However, currently there is no consensus on the roles of PHD2 in tumor progression and its specific mechanisms still require further elucidation. This review discusses the structural characteristics and the regulation of the PHD2 protein, and its roles in tumor angiogenesis, cell metabolism,malignant tumor phenotype, tumor immune microenvironment. Moreover, the progression in developing novel anti-tumor treatment strategies with the target of PHD was summarized. We aim to provide new strategies for further drug design and clinical research.
Stress granules (SGs) are dynamic membraneless organelles formed via liquid-liquid phase separation in cells under stress conditions (e.g., oxidative stress, hypoxia, viral infection). Composed primarily of mRNA and RNA-binding proteins, they are generally recognized as a cellular protective mechanism against external stimuli. Dysregulation of their homeostasis or persistent existence is closely linked to the development of various neurodegenerative diseases. This article systematically reviews the physiological and pathological functions of SGs, covering their formation mechanisms, core components, regulatory networks, and interactions with other organelles (e.g., mitochondria). It focuses on analyzing the dual role of SGs in neurodegenerative diseases, being both protective and pathogenic: On one hand, normally dynamic SGs protect neurons under acute stress by sequestering non-essential mRNA translation, promoting antioxidant defense, and inhibiting apoptotic signals. On the other hand, pathogenic factors associated with neurodegenerative diseases cause abnormal assembly, delayed disassembly, or impaired clearance (especially when autophagy is defective) of SGs, triggering their pathological "liquid-to-solid phase transition" into stable, cytotoxic solid aggregates (precursors of inclusion bodies). These abnormal SGs not only sequester key RNAs and proteins (including energy metabolism-related factors) to impair neuronal function, but also serve as core components of characteristic pathological inclusion bodies in neurodegenerative diseases. They form a vicious cycle by exacerbating protein homeostasis imbalance, mitochondrial dysfunction, and energy crisis, accelerating neuronal degeneration. This article elaborates the complex association between SGs and neurodegenerative diseases, particularly their mechanisms in early-stage diseases (e.g., RNA metabolism disorders, protein homeostasis imbalance), aiming to provide a key path for developing innovative diagnostic markers and intervention therapies.
Wilson disease (WD) is a disorder of copper metabolism caused by mutations in the ATP7B gene. Recent discoveries regarding dysfunction of the ubiquitin-proteasome system (UPS) and cuproptosis have provided new perspectives for elucidating its pathological mechanisms. This review proposes a reinforcing WD network, comprising copper overload resulting from ATP7B mutations, UPS dysfunction, and the cuproptosis pathway. We aim to offer a new theoretical framework for mechanistic research and targeted therapy of WD.
WANG Hao-Yun, WANG Si-Yuan, GE Yi-Dong, LI Yu-Xuan, KONG Li-Li, MAO Jia-Ning, CHEN Gun, CONG Ling-Hua, WANG Shu-Yan, YE Gang-Hui, YU Zong-Dong, LI Xin-Ming, JIN Jia-Bei, ZHAI Feng-Guang, ZHOU Zi-Jian, JIN Xiao-Feng, YE Meng
Analysis of TCGA and CPTAC datasets reveals that Kirsten rat sarcoma (KRAS) signaling is aberrantly upregulated in endometrial cancer (EC) and correlates with poor prognosis. However, the underlying mechanism remains unclear. Firstly, the expression of the KLHL14 gene in EC was analyzed using TCGA and CPTAC databases. Then the protein level of KLHL14 in human EC tissue samples was analyzed by immunohistochemistry. Then, the function of KLHL14 in HEC-1-A and Ishikawa cells was investigated by cell functional assays and xenograft tumor models. Finally, the protein levels of KLHL14-interacting proteins and KLHL14 downstream regulators in EC cells were detected by immunoprecipitation and immunofluorescence assays. Herein, we demonstrate that KLHL14, an E3 ubiquitin ligase substrate-binding adaptor, modulates the ubiquitination and degradation of the polymeric immunoglobulin receptor (PIGR), which mediates IgA transcytosis. Moreover, we found that KLHL14 is significantly elevated in EC and is negatively correlated with PIGR, with abnormally high KRAS signaling. In line with these findings, we found that KLHL14 overexpression dramatically promoted EC tumor growth in vivo, but not in vitro. Our findings reveal the underlying mechanism of KLHL14-induced EC progression by suppressing PIGR-mediated IgA transcytosis, providing a potential target for EC patients with high KRAS signaling.
Astaxanthin (AST), a natural carotenoid widely distributed in algae and aquatic animals, exhibits potent antioxidant activity. Previous studies have confirmed that AST can enhance the proliferation and differentiation of osteoblasts, thereby triggering new bone formation. However, it remains unclear whether AST exerts a protective effect on cadmium (Cd)-induced osteoblasts damage. Cellular senescence is an important mode of cell fate, which regulates the balance of bone metabolism and serves as a core therapeutic target for the treatment of bone metabolism-related diseases. The present study aims to investigate the protective effect of AST on Cd-induced osteoblasts damage and its underlying mechanisms. The results of MTT assay, lactate dehydrogenase (LDH) release assay, and Hoechst 33342/PI double staining showed that AST significantly inhibited Cd-induced osteoblasts death. Alkaline phosphatase (ALP) activity assay and alizarin red S staining demonstrated that AST markedly ameliorated Cd-induced abnormal differentiation of osteoblasts. The results of DCFH-DA staining, malondialdehyde (MDA) content detection, and superoxide dismutase (SOD) activity assay revealed that AST significantly reduced intracellular reactive oxygen species (ROS) production, decreased MDA contents, and increased SOD activity, thereby alleviating oxidative stress induced by Cd. Cell cycle analysis showed that AST reversed Cd-induced G0/G1 phase arrest in osteoblasts, leading to a significant decrease in the proportion of cells arrested in the G0/G1 phase. Senescence-associated β-galactosidase (SA-β-Gal) staining and enzyme-linked immunosorbent (ELISA) results showed that AST markedly reduced the number of SA-β-Gal-positive cells, while down-regulating the mRNA transcriptional and protein secretion levels of pro-inflammatory cytokines including IL-6 and IL-18, as well as matrix metalloproteinase-3 (MMP-3).Western blotting analysis demonstrated that AST significantly reversed the Cd-induced down-regulation of osteoblast differentiation-related marker proteins including collagen type I (Col I), Runt-related transcription factor 2 (RUNX2), as well as the proliferation-associated proteins proliferating cell nuclear antigen (PCNA) and cyclin D1; meanwhile, it inhibited the Cd-mediated up-regulation of cellular senescence-related proteins (p53, p21) and DNA damage-related protein phosphorylated γH2A.X (γH2A.X). Immunofluorescence staining indicated that AST significantly attenuated the abnormal accumulation of p21 protein in osteoblasts. In conclusion, AST exerts a protective effect on damaged osteoblasts by alleviating oxidative stress and attenuating Cd-induced osteoblasts senescence, suggesting that AST may be a candidate drug for the prevention and treatment of bone metabolic disorders caused by Cd exposure.
Drosophila visual transduction represents the fastest known G protein-coupled receptor (GPCR) signaling cascade, with its millisecond-scale response relying on highly compartmentalized photoreceptor structures and a precise signal regulatory network. As the first discovered member of the Myosin III family, NINAC fulfills essential roles in Drosophila visual signal termination and light adaptation through its splice variant p132. As a key calcium sensor, calmodulin (CaM) relies on its interaction with the p132 isoform of NINAC for its proper localization in the cytoplasm of photoreceptor cells. In this study, we successfully achieved soluble expression of the full-length p132 protein by using the Sf9 insect cell expression system. Size-exclusion chromatography coupled with multi-angle static light scattering (SEC-MALS) analysis demonstrated that high-homogeneity p132 monomers were obtained in the presence of ATP and Mg2+, confirming that ATP and Mg2+ are key factors in maintaining the stability of its monomeric conformation. The cryo-electron microscopy (cryo-EM) 2D classification results matched well with AlphaFold3-predicted structures at a low-resolution level,further confirming that the purified p132 protein possesses a relatively homogeneous conformation and stable state. GST pull-down assays indicated that the binding between full-length p132 and CaM is regulated by Ca2+. Using bio-layer interferometry (BLI) technique, the binding affinity between the p132 and CaM was measured to be 7.65 × 10-7 mol/L under Ca2+ conditions. In summary, this study represents the successful expression and purification of full-length monomeric p132. Preliminary structural analysis was performed, and the calcium-dependent interaction characteristics between p132 and CaM were elucidated. These findings establish a critical biochemical basis for future investigations into the full-length three-dimensional structure of the Drosophila p132/CaM complex, as well as its regulatory mechanisms and biological functions.
Depression imposes a substantial burden on global health and the economy; however, the extent to which varying degrees of depressive-like behavior influence gut microbiota composition and intestinal barrier function remains poorly understood. This study investigated the effects of depressive-like behaviors of differing severity that were induced by short-term or long-term restraint stress on multiple physiological systems in rats, including the hypothalamic-pituitary-adrenal (HPA) axis, intestinal inflammation, barrier integrity, gut microbiota composition, and short-chain fatty acid (SCFA) metabolism. Twenty-one male Sprague-Dawley rats were randomly assigned to three groups: a non-stressed control group, a short-term stress group (7 days) to model mild depression, and a long-term stress group (28 days) to model severe depression. Both stress-exposed groups exhibited depression-like behaviors, as evidenced by reduced locomotor activity in the open field test, decreased sucrose preference, and prolonged immobility in the forced swimming test, with the long-term stress group displaying significantly more pronounced deficits across all three measures. Stress exposure elevated serum corticosterone (CORT) and corticotropin-releasing hormone (CRH) levels, exacerbated colonic inflammation, and reduced both antioxidant markers (SOD, GSH-Px, T-AOC) and the expression ofintestinal barrier permeability-related proteins (MUC1, Claudin-1, ZO-1 and Occludin). Notably, all these changes were more pronounced in the severe depression group. Gut microbiota showed that mild depression markedly decreased gut microbial α-diversity and altered specific genera (e.g., reduced Holdemanella and Blautia, increased Clostridium_sensu_stricto_1), whereas severe depression further shifted taxa including Lachnospiraceae_NK4A136_group and Treponema_2. The observed microbial shifts correlated significantly with HPA axis activity, inflammation, and oxidative status, and were accompanied by disrupted fecal SCFA levels and receptor expression (GPR41/43/109A). Together, these findings establish depression severity as a key determinant of microbiota-gut-brain axis dysregulation and underscore the importance of timely intervention in stress-related disorders.
During the development of the inner ear, the Notch signaling pathway plays a central role in regulating the differentiation and development of supporting cells and hair cells in the inner ear. Irreversible damage to hair cells is the core factor leading to sensorineural hearing loss. This study used a single-layer attachment induction method and a matrix-free cell induction system to gradually differentiate human induced pluripotent stem cells into otic epithelial progenitors and hair cells, and upregulated the expression level of Jagged1 ligand at the OEPs stage. The expression of various cell marker genes, changes in the abundance of corresponding proteins, changes in ciliary structure on the surface of hair cells and changes in electrophysiological functions were multi-dimensionally detected to analyze the impact of Jagged1 gene overexpression on inner ear cell function. The results showed that compared with the control group infected with empty lentivirus, the overexpressed Jagged1 genome showed higher levels of OEPs (P<0.01), hair cell signature genes (P<0.001) and proteins (P<0.05). Both stereocilia and kinocilia were present on the cell surface, and scanning electron microscopy results showed that the number and the average length of stereocilia were both significantly increased (P<0.05). At the same time, it showed more mature hair cell electrophysiological functions, including L-type calcium current. It shows that the Jagged1 gene mainly plays a positive role in promoting the development and maturation of hair cells by promoting the differentiation of otic epithelial progenitors.
In recent years, immune checkpoint blockade represented by programmed death-1 (PD-1) and programmed death-ligand 1 (PD-L1) inhibitors has achieved major progress in liver cancer treatment. However, a subset of patients respond poorly, and the overall response rate remains limited. Aberrant accumulation of PD-L1 on the tumor cell membrane promotes immune evasion and limits immunotherapeutic efficacy, but the regulation of PD-L1 membrane homeostasis in liver cancer remains unclear. PRICKLE1 has been linked to tumor progression and membrane protein internalization. However, its role in PD-L1 trafficking is unknown. In this study, co-immunoprecipitation showed that endogenous PRICKLE1 interacts with PD-L1. PRICKLE1-stable overexpression and knockout cell lines were generated by plasmid overexpression and sgRNA-mediated intervention, respectively. In vitro assays further demonstrated that PRICKLE1 negatively regulates total and membrane PD-L1 protein levels. FM4-64 labeling and antibody internalization assays showed that PRICKLE1 enhances endocytic activity and promotes PD-L1 internalization. Immunofluorescence further revealed that PRICKLE1 facilitates trafficking of internalized PD-L1 to LAMP1-positive lysosomal compartments, while lysosomal inhibition reversed PRICKLE1-mediated PD-L1 downregulation, indicating lysosomal degradation. Public database and clinical sample analyses showed that PRICKLE1 is downregulated in liver cancer tissues and negatively correlates with PD-L1 expression. Collectively, PRICKLE1 reduces membrane PD-L1 abundance by promoting PD-L1 internalization and lysosomal degradation, suggesting PRICKLE1 as a potential target for intervening in immune evasion in liver cancer.
Mesodermal differentiation is a necessary step for the differentiation of pluripotent stem cells into cardiomyocytes. The transcription factor Brachyury T is the most classic marker gene of mesoderm and transiently expressed in cardiomyocyte differentiation. This study investigated the regulatory relationship between the expression of the Brachyury T gene and Wnt signaling. P19 teratocarcinoma stem cells were induced to differentiate into cardiomyocytes via suspension and adherent induction methods in the presence of dimethyl sulfoxide (DMSO). Quantitative real-time polymerase chain reaction (qRT-PCR) analysis showed that both Wnt3a and Brachyury T genes were transiently expressed exclusively at the mesodermal stage. Their expression levels under suspension induction were 2-3-fold higher than those under adherent induction. Treatment with Wnt agonists and inhibitors revealed that inhibition of Wnt signaling completely abolished Brachyury T gene expression, whereas Wnt activation also suppressed Brachyury T expression under suspension conditions but had minimal effects under adherent conditions. Promoter analysis demonstrated that the proximal promoter of Brachyury T contains evolutionarily conserved Wnt-responsive elements. Luciferase reporter assays further confirmed that Wnt activation enhanced the activity of the proximal Brachyury T promoter via the Wnt signaling pathway. Further analysis using a Brachyury T-GFP fusion construct showed that Wnt agonist and inhibitor treatments had little effect on the stability or nuclear localization of the fusion protein. In addition, overexpression of Brachyury T-GFP in P19 cells upregulated Wnt3a gene expression. Taken together, these findings indicate a reciprocal regulatory interaction between Brachyury T gene expression and Wnt signaling. Wnt signaling is required for Brachyury T expression, whereas excessive Wnt activity suppresses its expression. This regulatory pattern may be associated with the stage-specific characteristics of stem cell differentiation.
N6,2′-O-Dimethyladenosine (m6Am) is an important epitranscriptomic mark located near the RNA cap structure. It plays a key role in regulating mRNA stability, translation initiation, and interactions with RNA-binding proteins, and is closely associated with metabolic diseases as well as tumorigenesis and progression. Accurate identification of m6Am modification sites is of great significance for elucidating their molecular mechanisms and exploring diagnostic and therapeutic targets. However, existing prediction methods still have limitations in sequence context representation and position-dependent modeling. To improve the computational identification accuracy of RNA m6Am modification sites, this paper proposes a predictive model named im6Am-MPE, which integrates multiple position encodings with a residual multi-scale convolution-Transformer architecture. The model takes candidate sequences of length 41 nt as input and constructs feature representations by combining C2 encoding, nucleotide chemical property (NCP) encoding, as well as relative position, absolute position, and Gaussian position encodings. It then extracts local motif features via residual multi-scale one-dimensional convolution and captures long-range dependencies using a Transformer. Meanwhile, SE channel attention and Focal Loss are introduced to enhance feature expression and alleviate class imbalance. On two independent test sets, Full transcript and Mature RNA, the model achieves Accuracies (Acc) of 0.9557 and 0.9318, and Matthews correlation coefficients (MCC) of 0.6713 and 0.6877, respectively. The results demonstrate that the proposed method can effectively integrate local and global sequence information to improve the prediction performance of m6Am modification sites, providing an effective computational tool for RNA epitranscriptomic research.
Project-based learning (PBL) is a student-centered teaching model aiming to cultivate students’ abilities in inquiry, collaboration and practical application through the design and implementation of projects. To enhance the high-order, innovative, and challenging characteristics of the course and to develop a multifaceted evaluation system, we reformed the medical biochemistry practical teaching model based on PBL principle. A series of experimental projects were designed and conducted by students with a comprehensive research training process that includes preview reports, practical operations, problem-solving and achievement reporting. We also reformed the assessment methods at the same time, establishing a diversified evaluation system that integrates process-based evaluation and outcome-based assessment. This system places special emphasis on cultivating students’ innovative abilities, teamwork skills, and scientific thinking. The present study demonstrates that the project-based teaching model effectively enhances students’ self-directed learning ability, communication skills, and sense of cooperation, while also playing a significant role in the teaching of medical biochemistry practical courses. In conclusion, our study presents an effective strategy for improving the teaching of the medical biochemistry practical course.
In the context of China’s vigorous promotion of cross-disciplinary development, reform and innovation in biomedical interdisciplinary courses have become central tasks for the advancement of interdisciplinary fields and the cultivation of top-notch innovative talents. Exploring effective strategies for high-quality curriculum reform and practice is therefore essential for advancing disciplinary excellence. Taking the course “Biomedical Sensing and Measurement” at Zhejiang University as a representative case study, this paper systematically analyzes the common challenges faced by biomedical interdisciplinary courses, including complex curricular structures, difficulties in the design and implementation of the syllabus, and the challenge of balancing interdisciplinary innovative thinking with practical competence. Based on years of curriculum reform and teaching practice experience, the teaching team has established a four-in-one cultivation system of “curriculum framework-teaching model-practice-based education-collaborative ecosystem" centered on the core concept of “practice-cross discipline-innovation". Significant progress has been made in course outcomes, curriculum resources, teaching effectiveness, as well as the cultivation of interdisciplinary innovative thinking and practical skills. The authors systematically outline the pathways and innovative practices in cross-disciplinary curriculum reform aimed at cultivating interdisciplinary talents. The study could provide valuable insights for promoting interdisciplinary education and the training of versatile top-notch innovative talents in China.
The widespread application of digital intelligence technologies in education not only challenges traditional teaching models but also brings new opportunities for transformation to university educators. This study takes the "tricarboxylic acid cycle" in biochemistry as a case study to explore and implement an innovative teaching model driven by tasks and empowered by digital intelligence. Addressing the three major challenges in traditional teaching including difficulty in absorbing theoretical knowledge, disconnection from practical application, and the need to enhance higher-order thinking, the study proposes the teaching innovation framework of "dual integration and dual enhancement". This framework integrates digital-intelligent technologies with disciplinary frontiers while strengthening key and difficult concepts as well as ideological and political elements. A blended online and offline teaching cycle was constructed, covering pre-class, in-class, and post-class phases. By incorporating diverse teaching activities such as digital avatar dialogues, AI tools, virtual simulation experiments, molecular modeling competitions, and video/song creation, abstract metabolic knowledge was transformed into interactive and actionable embodied experiences. Teaching practice demonstrates that this model fully engages the initiative and participation of students, significantly improving their abilities in theoretical knowledge mastery, digital-intelligent skill application, innovative thinking, and engineering literacy. Simultaneously, the organic integration of ideological and political elements infuses value guidance into students’ scientific practice. This study not only provides concrete, actionable solutions to overcome teaching challenges in biochemistry but also offers a valuable reference model for advancing the digital-intelligent transformation of science and engineering courses and cultivating high-quality innovative talents.
To address the problems in the teaching of the Animal Biotechnology course, such as the inefficient translation of knowledge into competency, the theory-practice gap, and outdated course content, a systematic reform of the course was implemented based on the outcome-based education (OBE) concept. Following the principle of reverse design, the reform first defined the expected learning outcomes of students in terms of knowledge, skills, and qualities. The teaching content was then restructured through integration of cutting-edge technologies and industry cases. Diversified teaching methods combining flipped classroom, case-based teaching, and project-based learning were adopted. Furthermore, a whole process comprehensive assessment system incorporating both instructor and peer evaluation was established. Comparative analysis of grades showed that the post-reform cohort (Grade 2023, n=61) achieved a significantly higher average final score (81.2±7.1) than the pre-reform cohort (Grade 2022, n=58; 75.6±8.3) (P<0.01). Additionally, the excellence rate increased from 13.1% to 19.6%, while the failure rate dropped to zero. Questionnaire surveys revealed that over 70% of the students perceived a significant improvement in their literature retrieval and critical reading skills, depth of understanding of frontier technologies, and teamwork capabilities. The reform has successfully stimulated students’ learning initiative and interest, fostering the integration of knowledge, ability, and personal quality. These findings offer valuable insights for the development of similar courses.
Monthly journal, established in 1985 Sponsored by：
Chinese Society of Biochemistry and Molecular Biology
Peking University Undertaken by:
Peking University Health Science Center Edited by:
Editorial Office of Chinese Journal of Biochemistry and Molecular Biology Editor-in-Chief:
CHANG Zheng-Yi
ISSN 2097-4329 (Online)
ISSN 1007-7626 (Print)
CN 11-3870/Q
