Molecular and Cellular Biochemistry最新文献

{"title":"Skin regenerative potential of hydrogel matrices incorporated with stem cell-derived extracellular vesicles enriched with MicroRNAs: a systematic review.","authors":"Xiaolei Miao, Maryam Davoudi, Sahar Sadegh-Nejadi, Seyed Arsalan Ghahari, Molood Bagherieh, Reza Afrisham","doi":"10.1007/s11010-025-05248-5","DOIUrl":"10.1007/s11010-025-05248-5","url":null,"abstract":"<p><p>Stem cell-derived extracellular vesicles (SC-EVs) are one huge promise in skin regenerative medicine, similar in advantages to stem cells with low immunerejection and tumor formations. These microvesicles are laden with microRNAs, which assist in wound healing via angiogenesis and immune modulation. However, quick degradation and poor cellular uptake limit their regenerative capacity. Thanks to their adjustable characteristics, hydrogels can act as vehicles for transporting and sustainably releasing miRNA-SC-EVs at injury sites. Therefore, a systematic literature review was conducted on miRNA-enriched SC-EVs incorporated into hydrogels in animal skin regeneration models published from 2010 to 2024 (PROSPERO ID: CRD42024588072). Out of the 89 records, 12 met the criteria. Diabetic wounds are characterized by chronic inflammation, oxidative stress, and defective macrophage polarization, resulting in less satisfactory regeneration. The hydrogels tackled these issues by shifting macrophages from a pro-inflammatory M1 phenotype to a healing M2 phenotype, promoting collagen production, enhancing fibroblast movement, and boosting angiogenesis. Burn injuries frequently lead to slow recovery due to hypertrophic scarring, extended inflammation, and infection. Hyaluronic acid (HA)-derived hydrogels, infused with miR-21-5p and surface-treated with polydopamine and cationic antimicrobial peptides, promoted wound healing by lowering scarring and demonstrating anti-inflammatory, anti-apoptotic, and pro-angiogenic characteristics. The cell adhesion of these hydrogels can be enhanced by adding MOFs, chitosan, and extracellular matrix elements. The application of stimulus-responsive or stage-specific hydrogels is another mode of targeted healing. Further research and clinical trials will enhance the wound-healing efficiency of hybrid hydrogels.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4035-4067"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ZnT6-mediated Zn²⁺ redistribution: impact on mitochondrial fission and autophagy in H9c2 cells.","authors":"Erkan Tuncay, Yusuf Olgar, Leila Aryan, Suatnur Şık, Deniz Billur, Belma Turan","doi":"10.1007/s11010-025-05247-6","DOIUrl":"10.1007/s11010-025-05247-6","url":null,"abstract":"<p><p>Cytosolic free Zn²⁺ level ([Zn²⁺]_Cyt) is tightly regulated by Zn²⁺ transporters, under both physiological and pathological conditions. At the cellular level, dysregulated free Zn²⁺ levels have been linked to metabolic and cardiovascular diseases, primarily through their association with various Zn²⁺ transporters. However, the role and localization of ZnT6 in cardiomyocytes remain unclear. Previous studies have shown a significant increase in ZnT6 expression in insulin-resistant cardiomyocytes, suggesting a potential link between ZnT6 dysregulation and cardiac cell dysfunction. Therefore, here, we investigated the impact of ZnT6 overexpression (ZnT6-OE) on cellular Zn²⁺ distribution, mitochondrial dynamics, and autophagy-induced apoptosis in H9c2 cardiomyocytes. Using confocal imaging, biochemical assays, and electron microscopy, we demonstrated the mitochondrial localization of ZnT6 and its role in H9c2 cells. Our findings showed that ZnT6 overexpression led to a significant increase in mitochondrial free Zn²⁺ level ([Zn²⁺]_Mit) with a significant reduction in [Zn²⁺]_Cyt, which seems to be associated with enhanced numbers of mitochondria and mitochondrial fission process. Specifically, the ZnT6-OE cells exhibited increased dynamin-related protein 1 (DRP1) translocation to mitochondria which is an indication of excessive fission activity. We also determined severe mitochondrial dysfunction in ZnT6-OE cells, such as depolarization in mitochondrial membrane potential, production of excessive reactive oxygen species (ROS), reduced ATP levels, and autophagosome accumulation. Furthermore, these impairments were accompanied by elevated apoptotic markers, indicating autophagy-induced apoptosis. Our findings highlight ZnT6 as a critical regulator of mitochondrial dynamics and function in cardiomyocytes, contributing to disruption Zn²⁺ homeostasis by its overexpression, triggering excessive DRP1-mediated mitochondrial fission and leading to mitochondrial dysfunction, oxidative stress, and apoptotic cell death, suggesting an important impact of ZnT6 dysregulation on cardiomyocyte pathophysiology in metabolic disorders.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4283-4296"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143634298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prolonged sepsis triggers abnormal mitochondrial dynamics in the limb muscles and diaphragm.","authors":"Chao Xiong, Fasheng Guan, Jianguo Feng, Jing Jia, Jumei Zhang, Rui Tu, Jie Li, Jun Zhou, Jianglin Wang, Li Liu","doi":"10.1007/s11010-025-05338-4","DOIUrl":"https://doi.org/10.1007/s11010-025-05338-4","url":null,"abstract":"<p><p>Mitochondrial dysfunction is considered as a major trigger of sepsis-induced intensive care unit-acquired weakness (ICU-AW), but the precise role of impaired mitochondrial dynamics in sepsis-induced ICU-AW remains unclear. The cecal ligation and puncture (CLP) model was used to induce sepsis in mice. Fluid resuscitation and antibiotic treatment were used to establish a 5-day duration sepsis model, with sham-operated animals serving as controls. The muscle function of the diaphragm (DM) and tibialis anterior (TA) was assessed individually. Transmission electron microscopy (TEM) was used to observe changes in mitochondrial ultrastructure and measure the morphological parameters. Western blot analysis and quantitative real-time polymerase chain reaction were used to examine the expression of mitochondrial fusion and fission proteins and genes in DM and TA muscles. Additionally, inflammation and apoptosis were assessed in these muscles by measuring the level of pro-inflammatory cytokines and apoptotic DNA degradation, respectively. Mice subjected to CLP developed severe sepsis. Limb muscle dysfunction was more severe than that of the DM, as indicated by a greater reductions in compound muscle action potential, strength, fatigue index, and muscle fiber cross-sectional area. TEM analysis revealed sepsis-induced intermyofibrillar mitochondrial fragmentation and accumulation of injury. Both muscles showed reduced levels of Opa1 and Mfn2 mRNA and protein, and increased levels of Fis1 mRNA and protein. Correlation analysis revealed significant associations between muscle strength and Opa1, Mfn2, and Opa1/Drp1 at 5 days post-sepsis. Surviving mice at 5 days showed persistent inflammation, injury, and apoptosis in both muscles, but were more pronounced in the TA muscle. Prolonged sepsis leads to an impairment in mitochondrial dynamics, resulting in skeletal muscle weakness and atrophy, which may be one of the possible mechanisms of sepsis-induced ICU-AW.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: MMP1 3'UTR facilitates the proliferation and migration of human oral squamous cell carcinoma by sponging miR-188-5p to up-regulate SOX4 and CDK4.","authors":"Chengyong Wang, Chuanqing Mao, Yongzhen Lai, Zhiyu Cai, Weihui Chen","doi":"10.1007/s11010-025-05227-w","DOIUrl":"10.1007/s11010-025-05227-w","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4529"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143516158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of mitochondrial dysfunction in the protective effect of ginger derived extracellular vesicles on hepatic stellate cells against cytotoxicity.","authors":"Jing Yang, Yujie Yang, Xiqian Zhang, Yuan Qin, Toshihiro Sato, Shuyun Qing, Yirong Wang, Xiang Ye, Min Xu, Ying Liu, Qin He, Yaxian Zheng","doi":"10.1007/s11010-025-05232-z","DOIUrl":"10.1007/s11010-025-05232-z","url":null,"abstract":"<p><p>Previous studies have shown that ginger-derived extracellular vesicles (Gin-EVs) can alleviate alcohol-induced liver injury. It remained unknown and needs to be further verified that whether the vesicles has therapeutic potential to alleviate the progression of liver fibrosis. Moreover, the relevant mechanisms need to be further studied. Herein, we provide evidence that Gin-EVs effectively interact with human hepatic stellate cells (LX-2), offering protection against carbon tetrachloride (CCL4) or lipopolysaccharides (LPS)-induced liver fibrosis. The treatment with Gin-EVs was observed to mitigate fibrosis and enhance cell viability in LX-2 cells exposed to CCL4 or LPS. Mechanistically, Gin-EVs counteracted mitochondrial dysfunction by restoring mitochondrial dynamics imbalance characterized by enhanced fusion and reduced fission events while promoting mitochondrial biogenesis, thereby potentially preventing fibrotic processes in LX-2 cells. Collectively, the findings highlight the direct cytoprotective effects of Gin-EVs on LX-2 cells and suggest their promising role as a therapeutic option for hepatic fibrosis.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4297-4309"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis: a potential therapeutic target in cardio-cerebrovascular diseases.","authors":"Chenlong Jiang, Yang Yan, Tianlin Long, Jiawei Xu, Cuicui Chang, Meili Kang, Xuanqi Wang, Yuhua Chen, Junlin Qiu","doi":"10.1007/s11010-025-05262-7","DOIUrl":"10.1007/s11010-025-05262-7","url":null,"abstract":"<p><p>Cardio-cerebrovascular diseases (CCVDs) are the leading cause of global mortality, yet effective treatment options remain limited. Ferroptosis, a novel form of regulated cell death, has emerged as a critical player in various CCVDs, including atherosclerosis, myocardial infarction, ischemia-reperfusion injury, cardiomyopathy, and ischemic/hemorrhagic strokes. This review highlights the core mechanisms of ferroptosis, its pathological implications in CCVDs, and the therapeutic potential of targeting this process. Additionally, it explores the role of Chinese herbal medicines (CHMs) in mitigating ferroptosis, offering novel therapeutic strategies for CCVDs management. Ferroptosis is regulated by several key pathways. The GPX4-GSH-System Xc- axis is central to ferroptosis execution, involving GPX4 using GSH to neutralize lipid peroxides, with system Xc- being crucial for GSH synthesis. The NAD(P)H/FSP1/CoQ10 axis involves FSP1 regenerating CoQ10 via NAD(P)H, inhibiting lipid peroxidation independently of GPX4. Lipid peroxidation, driven by PUFAs and enzymes like ACSL4 and LPCAT3, and iron metabolism, regulated by proteins like TfR1 and ferritin, are also crucial for ferroptosis. Inhibiting ferroptosis shows promise in managing CCVDs. In atherosclerosis, ferroptosis inhibitors reduce iron accumulation and lipid peroxidation. In myocardial infarction, inhibitors protect cardiomyocytes by preserving GPX4 and SLC7A11 levels. In ischemia-reperfusion injury, targeting ferroptosis reduces myocardial and cerebral damage. In diabetic cardiomyopathy, Nrf2 activators alleviate oxidative stress and iron metabolism irregularities. CHMs offer natural compounds that mitigate ferroptosis. They possess antioxidant properties, chelate iron, and modulate signaling pathways like Nrf2 and AMPK. For example, Salvia miltiorrhiza and Astragalus membranaceus reduce oxidative stress, while some CHMs chelate iron, reducing its availability for ferroptosis. In conclusion, ferroptosis plays a pivotal role in CCVDs, and targeting it offers novel therapeutic avenues. CHMs show promise in reducing ferroptosis and improving patient outcomes. Future research should explore combination therapies and further elucidate the molecular interactions in ferroptosis.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4379-4399"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regional heterogeneity in vascular contractile dysfunction in diabetic mice.","authors":"Nada A Sallam, Ismail Laher","doi":"10.1007/s11010-025-05257-4","DOIUrl":"10.1007/s11010-025-05257-4","url":null,"abstract":"<p><p>Oxidative stress underlies many diabetic complications, including diabetic vasculopathy. It is unclear if oxidative stress has different effects in regionally distant arteries. We compared the contractile function of three arteries from diabetic mice and elucidated the mechanisms underlying their differential adaptation. We examined responses of the aorta, carotid and femoral arteries, isolated from the same diabetic (db/db) or normoglycemic control mice, to different vasoconstrictors in the presence and absence of indomethacin, apocynin, sulfaphenazole, L-NAME or a reactive oxygen species generating system to identify the enzyme(s) contributing to vascular dysfunction. Expression of superoxide dismutase (SOD) isoforms was measured. db/db aortae showed augmented contractile responses to KCl, phenylephrine, A23197 and U-46619 likely due to activated cyclooxygenases and hypersensitivity to thromboxane A2. Contractile responses of db/db carotid arteries were unaltered, likely due to higher SOD3 and SOD1 levels compared to the aortae. Femoral arteries were more vulnerable to oxidative stress, lacked SOD3 expression, and showed higher basal potassium channels activity. Phenylephrine contractions in femoral arteries were dependent on extracellular calcium entry; while contractions in aortae were dependent on extracellular calcium entry and intracellular calcium release. Femoral arteries from db/db mice exhibited higher basal potassium channels activity and attenuated contractility compared to control mice likely due to lower SOD levels. Heterogeneity exists between the three arteries at functional and molecular levels due to different signalling pathways and antioxidant defense mechanisms. Understanding regional differences in vasomotor control coupled with advanced delivery systems can help in developing therapies targeting specific vascular beds.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4513-4527"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144023645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SOX11 exacerbates ferroptosis to reduce lenvatinib resistance in liver cancer cells by promoting ubiquitination degradation of SREBF1 through upregulating UBE3A.","authors":"Zushun Chen, Lisong Ou, Liang Ma","doi":"10.1007/s11010-025-05218-x","DOIUrl":"10.1007/s11010-025-05218-x","url":null,"abstract":"<p><p>Lenvatinib is one of the most commonly used first-line drugs for liver cancer. However, lenvatinib resistance occurs in a large proportion of patients, posing a significant challenge. Ferroptosis, an iron-dependent form of cell death, plays a pivotal role in overcoming drug resistance. This study investigates the role of SRY-related HMG-box transcription factor 11 (SOX11) in regulating lenvatinib resistance in liver cancer through its impact on ferroptosis. qRT-PCR, western blot, and immunohistochemistry were performed to examine the expression of key molecules in patient samples and cell lines. Functional studies, including cell viability and proliferation assays, colony formation assays, flow cytometry, and measurements of iron metabolism markers, were conducted to explore the biological effects of these molecules. Additionally, Co-IP, ChIP, dual-luciferase reporter assays, and in vivo tumorigenesis experiments were performed to uncover the underlying regulatory mechanisms. Our results showed that UBE3A was markedly downregulated in lenvatinib-resistant liver cancer tissues and cells, and its overexpression markedly reduced lenvatinib resistance in liver cancer cells by promoting ferroptosis. Mechanically, UBE3A reduced lenvatinib resistance in lenvatinib-resistant liver cancer cells by mediating ubiquitination-independent degradation of SREBF1. In addition, SOX11 upregulation reduced lenvatinib resistance in liver cancer cells by promoting ferroptosis through transcriptionally activated UBE3A expression. In summary, SOX11 upregulation promoted ferroptosis in liver cancer cells by promoting SREBF1 ubiquitination degradation through transcriptionally elevating UBE3A expression, thereby sensitizing lenvatinib-resistant liver cancer cells to lenvatinib.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4119-4134"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High glucose facilitates hepatocellular carcinoma cell proliferation and invasion via WTAP-mediated HK2 mRNA stability.","authors":"Yongshen Niu, Siying Jia, Xuelian Xiao, Kangsheng Tu, Qingguang Liu","doi":"10.1007/s11010-025-05235-w","DOIUrl":"10.1007/s11010-025-05235-w","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is one of the most common cancers, and diabetes is a risk factor for hepatocarcinogenesis. N6-methyladenosine (m6A) methyltransferase WT1-associated protein (WTAP) is highly expressed in HCC and contributes to tumor progression. However, its role in high glucose-driven HCC progression remains unclear. The m6A quantitative assay was used to detect the m6A modification level. The levels of mRNAs and proteins were detected by qPCR, Western blot, and immunohistochemistry. CCK-8, colony formation, EdU, and transwell assays were used to detect HCC cell proliferation, invasion, and migration. Immunoprecipitation and CHX assays were used to reveal the regulatory effect of high glucose on WTAP. An RNA degradation experiment was used to explore WTAP's regulation of HK2 mRNA. To demonstrate the effect of high glucose on HCC growth in vivo, a diabetic mouse model was constructed, and HCC cells were subcutaneously injected. High glucose prominently increased the global level of m6A in HCC cells. Interestingly, high glucose upregulated WTAP protein rather than mRNA expression. We found that WTAP expression was significantly upregulated in HCC tissues, especially in tumor tissues of diabetic patients. WTAP knockdown markedly attenuated high glucose-induced abilities of HCC cell proliferation, colony formation, migration, and invasion. Meanwhile, WTAP overexpression significantly enhanced the malignant behaviors of HCC cells under low glucose conditions. High glucose reduced the ubiquitination of WTAP, thereby inhibiting its proteasomal and lysosomal degradation. Phosphorylated ERK (p-ERK) was required for high glucose-mediated WTAP stability. WTAP knockdown prominently abrogated high glucose-induced global m6A levels and HK2 expression in HCC cells. WTAP positively regulated HK2 expression by increasing mRNA stability. HK2 overexpression remarkably reversed the suppressive effects of WTAP knockdown on HCC cells. HK2 knockdown prominently abolished the promoting role of WTAP in HCC cells. Importantly, the growth of HCC cells in diabetic mice was significantly faster than that in control mice, which was prominently attenuated by WTAP knockdown. Our study demonstrated that high glucose decreased WTAP degradation and maintained its protein level by activating ERK phosphorylation. WTAP promoted HCC cell proliferation, colony formation, migration, and invasion by stabilizing HK2 mRNA.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4149-4168"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiomyocyte regeneration after infarction: changes, opportunities and challenges.","authors":"Ce Cao, Lili Yang, Jianshu Song, Zixin Liu, Haoran Li, Lei Li, Jianhua Fu, Jianxun Liu","doi":"10.1007/s11010-025-05251-w","DOIUrl":"10.1007/s11010-025-05251-w","url":null,"abstract":"<p><p>Myocardial infarction is a cardiovascular disease that poses a serious threat to human health. The traditional view is that adult mammalian cardiomyocytes have almost no regenerative ability, but recent studies have shown that they have regenerative potential under specific conditions. This article comprehensively describes the research progress of post-infarction cardiomyocyte regeneration, including the characteristics of cardiomyocytes and post-infarction changes, regeneration mechanisms, influencing factors, potential therapeutic strategies, challenges and future development directions, and deeply discusses the specific pathways and targets included in the regeneration mechanism, aiming to provide new ideas and methods for the treatment of myocardial infarction.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4015-4033"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}