Experimental cell research最新文献

{"title":"Maternal protein restriction impairs intestinal morphophysiology and antioxidant system in young male offspring rats","authors":"Isabela Baptista Leal dos Santos ,&nbsp;Matheus Naia Fioretto ,&nbsp;Miguel Silingardi Jorge ,&nbsp;Luísa Annibal Barata ,&nbsp;Isabelle Tenori Ribeiro ,&nbsp;André Matheus Leandro Franzolin ,&nbsp;Erick Guilherme Stoppa ,&nbsp;Renato Mattos ,&nbsp;Luiz Marcos Frediane Portela ,&nbsp;Maycon Tavares Emílio Silva ,&nbsp;Sérgio Alexandre Alcântara dos Santos ,&nbsp;José Ricardo de Arruda Miranda ,&nbsp;Clélia Akiko Hiruma Lima ,&nbsp;Luis Antonio Justulin","doi":"10.1016/j.yexcr.2025.114464","DOIUrl":"10.1016/j.yexcr.2025.114464","url":null,"abstract":"<div><div>The developmental origins of health and disease (DOHaD) concept suggests that adverse conditions during gestation can influence the development and function of multiple organs, including the gastrointestinal tract. Maternal protein restriction (MPR) exposure has been associated with negative effects on reproduction, the endocrine system, and liver metabolic health. However, limited research has explored the impact of MPR on the offspring's intestinal morphophysiology. This study investigated the effects of gestational and lactational MPR on the duodenum and colon of young male offspring rats at postnatal (PND)21. We hypothesize that MPR affects intestinal morphophysiology and development early in life. Our findings revealed tachygastria in offspring exposed to MPR. The ultrastructural analysis uncovered a reduction in goblet cell numbers and changes in collagen deposition in the duodenum and colon. We also identified imbalances in inflammatory markers (IL-6 and TGF-β1) and antioxidant enzymes (CAT and SOD). These results demonstrate that MPR significantly affects gastrointestinal morphophysiology early in life by disrupting gastric motility and altering duodenal and colonic histoarchitecture, antioxidant defense, and inflammatory pathways. Such alterations may predispose the descendants to long-term gastrointestinal disorders, underscoring the importance of further research on the developmental origins of intestinal health and disease.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114464"},"PeriodicalIF":3.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143471263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeted inhibition of NPR3/MAPK pathway enhances dental pulp stem cell multipotency: Mechanistic validation based on ligustrazine (TMP)","authors":"Hailiang Cui ,&nbsp;Yeying Zhang ,&nbsp;Huiling Liang ,&nbsp;Lizheng Wu","doi":"10.1016/j.yexcr.2025.114479","DOIUrl":"10.1016/j.yexcr.2025.114479","url":null,"abstract":"<div><h3>Background</h3><div>The multipotency of dental pulp stem cells (DPSCs) plays a crucial role in dental tissue regeneration, yet its regulatory mechanisms remain incompletely understood. This study aimed to investigate the role of natriuretic peptide receptor 3 (NPR3) in regulating DPSCs functions and validate the mechanism of its targeted inhibitor ligustrazine (TMP).</div></div><div><h3>Methods</h3><div>NPR3 expression in DPSCs was examined by Western blot and immunohistochemistry. The effects of NPR3 on DPSCs colony formation, migration, and differentiation were investigated through overexpression and knockdown strategies. The relationship between NPR3 and ERK1/2 pathway was explored using molecular biological approaches. High-throughput drug screening was employed to identify TMP as an NPR3 inhibitor, followed by mechanism validation.</div></div><div><h3>Results</h3><div>NPR3 was highly expressed in mature odontogenic DPCs, with its expression levels closely correlated with DPSCs functions. Functional assays demonstrated that NPR3 inhibited DPSCs colony formation, migration, and differentiation capabilities, while NPR3 knockdown significantly enhanced these functions. Mechanistic studies revealed that NPR3 influenced DPSCs functions through positive regulation of ERK1/2 phosphorylation. Through high-throughput screening, we identified TMP as a specific NPR3 inhibitor that promoted DPSCs functions. Rescue experiments further confirmed that NPR3 overexpression or ERK1/2 inhibitor SCH772984 attenuated TMP-induced enhancement, validating TMP's action through the NPR3/MAPK pathway.</div></div><div><h3>Conclusion</h3><div>This study reveals the crucial role of the NPR3/MAPK pathway in regulating DPSCs multipotency and demonstrates that TMP enhances DPSCs functions through targeted inhibition of this pathway, providing new therapeutic strategies and drug targets for dental tissue regeneration.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114479"},"PeriodicalIF":3.3,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143464276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a biomarker panel for cell characterization intended for cultivated meat","authors":"Marc Auguet-Lara,&nbsp;Stig Skrivergaard,&nbsp;Margrethe Therkildsen,&nbsp;Martin Krøyer Rasmussen ,&nbsp;Jette Feveile Young","doi":"10.1016/j.yexcr.2025.114467","DOIUrl":"10.1016/j.yexcr.2025.114467","url":null,"abstract":"<div><div>Cultivated meat has in recent years been suggested as a sustainable alternative to produce meat at large-scale. Several aspects of cultivated meat production have demonstrated significant progress. However, there are still many questions regarding the cell culture, media composition, and the production itself to be answered and optimized. Finding good starter cell populations is a challenge to address and requires robust tools to characterize the cell populations. Detailed analysis is required to identify each type of cell within the skeletal muscle niche leads to optimized cultivated meat production at large-scale. In this study, we developed a set of biomarkers, using digital droplet PCR (ddPCR) and Immunofluorescence (IF) staining, to identify specific cell types within a heterogeneous cell population isolated from skeletal muscle tissue. We showed that combining Neural Cell Adhesion Molecule (NCAM), Calponin 1 (CNN1), and Fibronectin (FN), can be a powerful approach to predict the growth of skeletal myotubes, smooth muscle mesenchymal cells (SMMCs), and myofibroblasts, respectively. Moreover, early cell-cell interactions of fibroblastic cells were observed to be triggered through thin actin filaments containing CNN1 protein, to form, subsequently, myofibroblast networks. Besides, Myogenic Differentiation 1 (MyoD) is the key marker to detect skeletal muscle growth, whereas Myogenic Factor 5 (MyF5) can be expressed in myogenic and non-myogenic cells. MyF5 was detected at differentiation stages within the myotube nuclei, suggesting an unknown role during myotube formation.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114467"},"PeriodicalIF":3.3,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143445719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HOXD8 Drives Glioma Progression through Epithelial-Mesenchymal Transition Regulation: Implications for Prognosis and Targeted Therapy.","authors":"Ke Yu, Jiawei Meng, Tiange Chen, Yanshi Wang, Yi Zhao, Tianxiang Huang, Ge Gao","doi":"10.1016/j.yexcr.2025.114476","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114476","url":null,"abstract":"<p><p>Glioma is one of the most common primary malignant tumors of the central nervous system. Here, we defined Homeobox D8 (HOXD8) as a novel biomarker for glioma utilizing RNA-sequencing and bioinformatics approaches. HOXD8 expression was significantly upregulated in glioma cell lines (U251 and U373) and clinical specimens compared to normal controls. Functional studies demonstrated that HOXD8 knockdown markedly inhibited glioma cell proliferation, migration, and invasion in vitro. Additionally, pan-cancer analysis revealed significant associations between HOXD8 expression and key tumor characteristics, including immune cell infiltratio, tumor mutational burde, and microsatellite instability. Meanwhile, transcriptomic profiling and pathway analysis identified HOXD8's involvement in epithelial-mesenchymal transition (EMT) regulation, with western blot validation showing significant modulation of EMT markers following HOXD8 knockdown. Collectively, our results suggests that HOXD8 may serve as a satisfactory prognostic biomarker that promotes glioma cell proliferation, migration and invasion,potentially through regulation of EMT processes.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114476"},"PeriodicalIF":3.3,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A new mechanism in steroid-induced osteonecrosis of the femoral head and the protective role of simvastatin","authors":"Xu-huan Li ,&nbsp;Shi-da Qian ,&nbsp;Dan Chen ,&nbsp;Zhou-zhou Li ,&nbsp;Kai-yun Chen ,&nbsp;Yong-ping Pan ,&nbsp;Xiu-hua Lv ,&nbsp;Run-qing Jia ,&nbsp;Xue-feng Yu","doi":"10.1016/j.yexcr.2025.114471","DOIUrl":"10.1016/j.yexcr.2025.114471","url":null,"abstract":"<div><h3>Objective</h3><div>Steroid-induced osteonecrosis of the femoral head (SONFH) is a debilitating bone condition associated with femoral head collapse and hip joint dysfunction. The pathogenesis of SONFH is still not fully elucidated. This study aims to explore the role of mitochondrial cardiolipin metabolism disruption in SONFH and the potential protective effects of simvastatin (SIM).</div></div><div><h3>Methods</h3><div>Osteoblasts were cultured in vitro under high concentrations of dexamethasone (DEX) to mimic the effects of glucocorticoid exposure seen in SONFH. Mitochondrial structural changes and cardiolipin distribution were examined using transmission electron microscopy and confocal microscopy. Osteoblast proliferation and apoptosis were assessed using CCK-8 assays and flow cytometry. Mitochondrial cardiolipin content was quantified by ELISA, while cytochrome <em>c</em> (Cyt-c) expression was measured through Western blotting. Mitochondrial staining with NAO was analyzed using confocal microscopy and flow cytometry.</div></div><div><h3>Results</h3><div>DEX exposure led to mitochondrial cardiolipin metabolism disorder and redistribution, resulting in significant mitochondrial structural damage. This disruption was associated with increased release of Cyt-c into the cytoplasm, which correlated with heightened osteoblast apoptosis. SIM treatment mitigated these effects, reducing osteoblast apoptosis by preserving mitochondrial function and modulating cardiolipin content and distribution.</div></div><div><h3>Conclusion</h3><div>This study demonstrates, for the first time, that glucocorticoid-induced disruptions in mitochondrial cardiolipin metabolism contribute to the pathogenesis of SONFH by inducing Cyt-c release and subsequent osteoblast apoptosis. SIM exerts a protective effect by preserving mitochondrial integrity and function, offering a potential therapeutic avenue for treating hormone-induced osteoblast damage in SONFH.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114471"},"PeriodicalIF":3.3,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143464277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring mitonuclear interactions in the regulation of cell physiology: insights from interspecies cybrids.","authors":"Kateryna Gaertner, Riikka Tapanainen, Sina Saari, Zsófia Fekete, Steffi Goffart, Jaakko L O Pohjoismäki, Eric Dufour","doi":"10.1016/j.yexcr.2025.114466","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114466","url":null,"abstract":"<p><p>Brown hares (Lepus europaeus) and mountain hares (Lepus timidus) frequently hybridize in regions where their range overlaps, producing fertile offspring and enabling gene flow between the species. Despite this, no hybrid species has emerged, suggesting that hybrid backcrosses may incur fitness costs. One potential mechanism for such costs involves the interactions between mitochondrial and nuclear gene products, where incompatibilities between species-specific alleles may reinforce species barriers and lead to hybrid breakdown. However, direct experimental evidence for this hypothesis remains limited. In this study, we used fibroblasts derived from skin biopsies of wild-caught hares to generate cytoplasmic hybrid (cybrid) cell lines, wherein mitochondria and mtDNA from one species were transferred to mitochondria-depleted cells of the other species, creating novel mitonuclear gene combinations while preserving the original diploid nuclear background. Employing a range of techniques - including transcriptomics, metabolomics, microscopy, and respirometry - we explored the consequences of mitochondrial transfer between these hare species. Our results reveal that in the studied species mitonuclear incompatibilities exhibit strong effects on cellular fitness but are limited to specific genotypes. We propose mechanisms of cellular-level incompatibility and their potential consequences for interspecific hybrids, offering new insights into the complexity of mitonuclear interactions.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114466"},"PeriodicalIF":3.3,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A genome-wide CRISPR-Cas9 knockout screen using dynamin knockout cells identifies Nf2 and Traf3 as genes involved in dynamin-independent endocytosis.","authors":"Sho Takahashi, Mizuho Maehara, Chihiro Nishihara, Hiroyuki Iwata, Shusaku Shibutani","doi":"10.1016/j.yexcr.2025.114470","DOIUrl":"https://doi.org/10.1016/j.yexcr.2025.114470","url":null,"abstract":"<p><p>Endocytosis is a fundamental process by which cells take up extracellular materials, including nutrients, growth factors, and pathogens. Although several endocytic pathways, such as clathrin-mediated and caveolin-mediated endocytosis, are well-characterized, other endocytic pathways remain poorly understood. Therefore, in this study, we performed a genome-wide CRISPR-Cas9 screen to elucidate new endocytic pathways using dynamin conditional knockout cells. We identified genes that significantly reduced the cell numbers when knocked out simultaneously with dynamin. Among these, neurofibromin 2 (Nf2) and tumor necrosis factor receptor-associated factor 3 (Traf3), whose relationship with endocytosis was not well understood, were investigated for their roles in endocytosis activity. Nf2 and Traf3 knockout cells exhibited reduced non-specific fluid endocytosis in a dynamin-independent manner. However, Nf2 or Traf3 knockout did not affect the transferrin receptor-mediated endocytosis that depends on clathrin and dynamin. Moreover, Nf2 knockout cells showed reduced cholera toxin uptake in a dynamin-independent manner. Overall, this study highlights the roles of Nf2 and Traf3 in endocytosis.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114470"},"PeriodicalIF":3.3,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRIM22 inhibits the metastasis of colorectal cancer through facilitating β-Catenin degradation","authors":"Haiyang Hu,&nbsp;Wensheng Li,&nbsp;Pengfei Ma,&nbsp;Junxin Song,&nbsp;Xiaobo Zhang,&nbsp;Longhui Ruan,&nbsp;Jing Zhang,&nbsp;Youwei Zheng","doi":"10.1016/j.yexcr.2025.114473","DOIUrl":"10.1016/j.yexcr.2025.114473","url":null,"abstract":"<div><div>Tripartite motif-containing 22 (TRIM22), a member of the tripartite motif protein family, has emerged as a putative tumor suppressor in various cancers. Nevertheless, its specific role and clinical significance in colorectal cancer (CRC) remain poorly characterized. Herein, we observed that TRIM22 expression was frequently downregulated in primary CRC tissues and was significantly correlated with better prognosis. Functional assays demonstrated that TRIM22 overexpression substantially attenuated the metastatic potential of CRC cells both in vitro and in vivo. Mechanistically, our results revealed that TRIM22 directly interacts with and ubiquitinates β-Catenin, a crucial transcription factor that drives CRC metastasis by modulating the epithelial-mesenchymal transition (EMT) process. Additionally, our data indicated that the anti-metastatic effect of TRIM22 relies on the degradation of β-catenin. In summary, this study is the first to deliberate the vital anti-tumor role of TRIM22 in CRC metastasis. We also provide new evidence suggesting that TRIM22 could be a prognostic marker and therapeutic target for inhibiting CRC progression.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114473"},"PeriodicalIF":3.3,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Allograft inflammatory Factor-1 induces the dedifferentiation of Vascular Smooth Muscle cells into a macrophage-like phenotype both in vivo and in vitro","authors":"Ruoyu Dong ,&nbsp;Jikuan Li ,&nbsp;Guangwei Jiang ,&nbsp;Yunjie Tian ,&nbsp;Wei Bi","doi":"10.1016/j.yexcr.2025.114475","DOIUrl":"10.1016/j.yexcr.2025.114475","url":null,"abstract":"<div><div>Atherosclerosis, a chronic lipid-driven vascular inflammatory disease involving multiple cell types, is the primary cause of cardiovascular disease-related morbidity and mortality. Allograft inflammatory factor 1 (AIF-1) contributes to atherosclerosis development by affecting vascular smooth muscle cells (VSMCs). Increasing research indicates that VSMCs are pivotal in atherosclerosis progression, particularly in macrophage-like phenotypic switching, though the mechanism of AIF-1 VSMCs phenotypic switching is not well understood. This study aims to correlate AIF-1 expression with atherosclerosis development and VSMCs phenotypic switching. AIF-1 was expressed in the atherosclerotic plaques of patients with carotid artery narrowing and atherosclerosis mice. AIF-1 was expressed in ox-LDL treated VSMCs and promoted the apoptosis of VSMCs. AIF-1 significantly influenced macrophage-like VSMC numbers through the AIF-1/NF-κB pathway, enhancing lipid uptake and TNF-α and IL-6 secretion. This study showed increased AIF-1 expression in atherosclerotic plaques in both patients with carotid stenosis and an atherosclerosis animal model. AIF-1 facilitated VSMC dedifferentiation into macrophage-like cells, enhancing lipid uptake and inflammatory factor release through the AIF-1/NF-κB pathway.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114475"},"PeriodicalIF":3.3,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NRF-1 promotes FUNDC1-mediated mitophagy as a protective mechanism against hypoxia-induced injury in cardiomyocytes","authors":"Junliang Li ,&nbsp;Hui Li ,&nbsp;Nan Niu ,&nbsp;Yazhou Zhu ,&nbsp;Siyu Hou ,&nbsp;Wei Zhao","doi":"10.1016/j.yexcr.2025.114472","DOIUrl":"10.1016/j.yexcr.2025.114472","url":null,"abstract":"<div><div>Hypoxia-induced apoptosis and mitochondrial dysfunction in cardiomyocytes are involved in the mechanisms of heart failure. Our previous studies have confirmed that NRF-1 alleviates hypoxia-induced injury by promoting mitochondrial function and inhibiting apoptosis in cardiomyocytes. However, the mechanism by which NRF-1 attenuates hypoxia-induced injury in cardiomyocytes is still unclear. Mitophagy, a selective autophagy, has recently shown a remarkable correlation with hypoxia-induced cardiomyocyte injury. In this study, we evaluated whether NRF-1 protects cardiomyocytes from hypoxia-induced injury by regulating mitophagy. The findings indicate that hypoxia prevents H9c2 cells from growing, encourages mitochondrial dysfunction, and triggers mitophagy. In addition, promoting mitophagy by rapamycin reduces hypoxia-induced injury in H9c2 cells. Overexpression of NRF-1 in hypoxia-induced H9c2 cells promotes mitophagy and alleviates cell injury, and this effect can be inhibited by 3-MA. Further study found that NRF-1 promotes the expression of FUNDC1 by binding to its promoter region. Knockdown of FUNDC1 in NRF-1 over-expression H9c2 cells inhibited mitophagy and aggravated hypoxia-induced injury. In conclusion, our study suggests that NRF-1 protects against hypoxia-induced injury by regulating FUNDC1-mediated mitophagy in cardiomyocytes.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114472"},"PeriodicalIF":3.3,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143454306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}