JOURNAL OF CELLULAR AND MOLECULAR MEDICINE最新文献

{"title":"DNA Methylation Regulatory Axis miR-29b-3p/DNMT3B Regulates Liver Regeneration Process by Altering LATS1","authors":"Yinwen Zhou,&nbsp;Hao Wu,&nbsp;Qiu Wang,&nbsp;Bo Ma,&nbsp;Jiulong Sun,&nbsp;Guoliang Wang","doi":"10.1111/jcmm.70405","DOIUrl":"https://doi.org/10.1111/jcmm.70405","url":null,"abstract":"<p>DNA methylation is a crucial epigenetic alteration involved in diverse biological processes and diseases. Hippo signalling pathway is a key signalling regulatory network in the growth and development of tissues and organs. Nevertheless, the precise role of DNA methylation and Hippo signalling pathway during liver regeneration (PH) is still unclear. In this study, we investigated the regulatory mechanism of LATS1, a pivotal protein in the Hippo signalling pathway, on liver regeneration and explored the specific mechanism of DNA methylation regulating LATS1. To analyse the regulation of LATS1 by DNA methylation, following 2/3 partial hepatectomy (PH) in liver-specific AAV-8 shDNMT3B deleted mice (<i>DNMT3B</i>, KD) mice and sex-matched AAV-8 shControl (Control). We determined that DNMT3B regulates the protein expression of LATS1 by DNA methylation. miR-29b-3p significantly regulates the expression of DNMT3B and alters LATS1 expression to inactivate the Hippo signalling pathway, thereby reducing the expression of cell proliferation and cycle proteins and inhibiting liver regeneration. Our results indicated that the miR-29b-3p/DNMT3B regulatory axis influences LATS1 expression through DNA methylation, and thereby promotes liver regeneration.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70405","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143389225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “TAK1 mediates excessive autophagy via p38 and ERK in cisplatin-induced acute kidney injury”","authors":"","doi":"10.1111/jcmm.70414","DOIUrl":"https://doi.org/10.1111/jcmm.70414","url":null,"abstract":"<p>Zhou J, Fan Y, Zhong J, et al. TAK1 mediates excessive autophagy via p38 and ERK in cisplatin-induced acute kidney injury. <i>Journal of cellular and molecular medicine</i> 2018;22(5):2908–2921. doi:10.1111/jcmm.13585.</p><p>In Zhou Jun et al., the immunohistochemistry (IHC) image for sham in Figure 1H was inadvertently misused during the figure preparation process. This correction does not affect the figure legends or the conclusions drawn in the study. The correct figures are shown below.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70414","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143389241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Renal Lipid Alterations From Diabetes to Early-Stage Diabetic Kidney Disease and Mitophagy: Focus on Cardiolipin","authors":"Zhijie Li,&nbsp;Hongmiao Wang,&nbsp;Nan Liu,&nbsp;Xiayuchen Lan,&nbsp;Ailing Xie,&nbsp;Ge Yuan,&nbsp;Bowen Li,&nbsp;Jiaxin Geng,&nbsp;Xiaodan Liu","doi":"10.1111/jcmm.70419","DOIUrl":"https://doi.org/10.1111/jcmm.70419","url":null,"abstract":"<p>Lipotoxicity plays a crucial role in the progression of diabetic kidney disease (DKD), yet the dynamic changes in renal lipid composition from diabetes to early-stage DKD remain unclear. Free fatty acids, lactosylceramides and cardiolipin (CL) were identified as the most significantly altered lipids by quantitatively comparing targeted lipids in the renal cortex of the classic spontaneous diabetic <i>db/db</i> mice using high-coverage targeted lipidomics. Further investigation into the causes and effects of decreased CL, which is a unique mitochondrial phospholipid, was conducted in mitochondria-rich renal proximal tubular cells by using western blotting, real-time PCR, immunohistochemistry and transmission electron microscopy. Reduced expression of cardiolipin synthase, a key enzyme in the CL synthesis pathway, and inhibition of CL-related mitophagy were confirmed under high glucose conditions. In addition, the protective effect of CL-targeted Szeto-Schiller 31 in preserving mitophagy was demonstrated in both in vivo and in vitro studies. These findings provide new insights into the pathogenesis of early-stage DKD from a lipid perspective and offer a theoretical basis for discovering new treatments.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70419","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143389224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bu Yang Huan Wu Prevents Osteogenic Effect of Muscle-Derived Stromal Cells via Regulating JAK/STAT Pathway","authors":"Guorui Cao,&nbsp;Shaoyun Zhang,&nbsp;Yuanping Liao,&nbsp;Chen Yue,&nbsp;Lanbo Yang,&nbsp;Jiayi Guo,&nbsp;Peijian Tong,&nbsp;Honglue Tan","doi":"10.1111/jcmm.70413","DOIUrl":"https://doi.org/10.1111/jcmm.70413","url":null,"abstract":"<p>Heterotopic ossification (HO) is a crucial pathological process in which bone or calcification develop in skeletal muscle and surrounding soft tissues. Muscle-derived stromal cells (MDSC) are important muscle-resident mesenchymal progenitor cells and macrophage-derived oncostatin M (OSM) can induce osteogenic differentiation. Bu Yang Huan Wu (BYHW), which has a long history of use in restraining inflammation, can prevent osteogenic differentiation and HO formation while underlying mechanism is still unclear. The Janus kinase/signal transducer and activator of transcription (JAK/STAT) signalling pathway is an important pathway to regulate osteogenic differentiation of related cells. In this study, we investigated whether BYHW could inhibit osteogenesis effect of MDSC through OSM mediated by macrophages, and whether JAK/STAT pathway regulated this biological process. We found that activated macrophages promoted osteogenic differentiation of MDSC through OSM and BYHW could decrease the level of OSM and osteogenic activity of MDSC. Further, we confirmed the regulatory effect of JAK/STAT pathway, blocking this pathway could suppress the level of OSM and osteogenic differentiation of MDSC. We showed that BYHW could suppress osteogenic differentiation of MDSC through JAK/STAT signalling. These findings expand the application scope of traditional Chinese medicine and provide a basis for the further investigation of the potential therapeutic role of HO.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70413","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143389421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progress in Research on Regulated Cell Death in Cerebral Ischaemic Injury After Cardiac Arrest","authors":"Zumin Chen,&nbsp;Shuangwei Wang,&nbsp;Tian Shu,&nbsp;Senlin Xia,&nbsp;Yanmei He,&nbsp;Yanhan Yang","doi":"10.1111/jcmm.70404","DOIUrl":"https://doi.org/10.1111/jcmm.70404","url":null,"abstract":"<p>Ischaemic damage to the brain is the main cause of brain injury after cardiac arrest. The current treatment focuses on early reperfusion, but reperfusion tends to cause reperfusion injury, which is a significant problem. Cell death is an irreversible and normal end to cell life, playing key roles in maintaining the homeostasis and development of multicellular organisms. To date, cell death can be classified into two categories: accidental cell death (ACD) and regulated cell death (RCD). Cell death plays an indispensable role in cerebral ischaemia injury. An increasing number of scholars are exploring the mechanisms and sites of cell death during targeted inhibition of cerebral ischaemia to treat cerebral ischaemia injury. In addition to the established cell death pathways, namely, the apoptosis, pyroptosis and necroptosis pathways, ferroptosis and cuproptosis pathways have been discovered. This article reviews the cell death pathways involved in ischaemic brain injury, discusses the roles played by these death modalities, and suggests therapeutic directions for future targeting of cell death sites.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70404","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143389371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiotensin-(1–9) Improves the Cardioprotective Effects of Del Nido Cardioplegia Against Ischemia/Reperfusion Injury","authors":"Evelyn Mendoza-Torres,&nbsp;Gina Sanchez,&nbsp;Wendy Rosales,&nbsp;María Clara Ospino,&nbsp;Luis Antonio Díaz-Ariza,&nbsp;Yuliet Montoya,&nbsp;John Bustamante,&nbsp;Jaime A. Riquelme,&nbsp;Mario Chiong,&nbsp;Sergio Lavandero","doi":"10.1111/jcmm.70412","DOIUrl":"https://doi.org/10.1111/jcmm.70412","url":null,"abstract":"<p>Del Nido cardioplegia (DNC), a blood-and-crystalloid solution containing high and low concentrations of potassium and calcium, respectively, is used as a single-dose antegrade infusion to induce immediate cardiac arrest in the surgery of patients with cardiovascular diseases requiring extracorporeal circulation. Adding cardioprotective molecules may further reduce the damage-triggered ischemia/reperfusion (I/R) injury. Angiotensin-(1–9) (Ang-(1–9)) and angiotensin-(1–7) (Ang-(1–7)), members of the counter-regulatory renin-angiotensin system, have shown cardioprotective effects in cardiac hypertrophy and I/R models. This study aimed to evaluate the effects of Ang-(1–9) and Ang-(1–7), as adjuvants of the DNC, on cardioprotection and ventricular function in isolated rat hearts subjected to I/R and in cultured neonatal rat ventricular myocytes subjected to simulated I/R (sI/R). The addition of DNC and Ang-(1–9) and Ang-(1–7) decreased lactic dehydrogenase (LDH) release in cultured cardiomyocytes subjected to sI/R in comparison to those cardiomyocytes subjected to sI/R and incubated with DNC alone. Moreover, hearts treated with Ang-(1–9) during reperfusion after DNC + I/R exhibited fewer arrhythmias and required less time to reach left ventricular developed pressure stability. Overall, reperfusion with DNC and Ang-(1–9) improves the recovery of the left ventricular function of the heart.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70412","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143389240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to ‘ARID1A downregulation promotes cell proliferation and migration of colon cancer via VIM activation and CDH1 suppression’","authors":"","doi":"10.1111/jcmm.70191","DOIUrl":"https://doi.org/10.1111/jcmm.70191","url":null,"abstract":"<p>Baldi S, Zhang Q, Zhang Z, et al. ARID1A downregulation promotes cell proliferation and migration of colon cancer via VIM activation and CDH1 suppression. <i>J Cell Mol Med.</i> 2022;26:5984-5997. doi:10.1111/jcmm.17590.</p><p>In Salem Baldi et al., the VIM image of HCT116 cells in Figure 5B overlapped the VIM in Figure 5A due to technical error during image preparation. The correct figure is shown below. The authors confirm all results and conclusions of this article remain unchanged.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70191","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143380550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the Axis of Gut Microbiota-Inflammatory Cytokine-Atrial Fibrillation in the Pathogenesis of Atrial Fibrillation","authors":"Jun Chen,&nbsp;Yucheng Wang,&nbsp;Kangnan Wang,&nbsp;Ziwei Mei,&nbsp;Lihong Wang","doi":"10.1111/jcmm.70379","DOIUrl":"https://doi.org/10.1111/jcmm.70379","url":null,"abstract":"<p>A relationship may exist between the gut microbiota, inflammatory factors and atrial fibrillation (AF); however, the precise biological mechanisms linking these components remain uncertain.In this study, 211 single-nucleotide polymorphisms associated with the gut microbiota were collected from the MiBioGen consortium. Summary data for AF were sourced from large-scale genome-wide association studies. Two-step Mendelian randomization (MR) was applied to estimate the possible mediating effect of inflammatory cytokines on the causality between the gut microbiota and AF. MR confirmed the effects of class Lentisphaeria, family Bifidobacteriaceae, family XIII, genus <i>Anaerostipes</i>, genus <i>Howardella</i>, genus <i>Intestinibacter</i>, genus <i>Lachnospiraceae</i> (NK4A136 group), genus <i>Odoribacter</i>, genus <i>Ruminococcus gnavus</i>, order Bifidobacteriales, order Victivallales and phylum Lentisphaerae on AF prevention. Moreover, MR revealed the role of Fms-related tyrosine kinase 3 ligand, interleukin-6, interleukin-7, leukaemia inhibitory factor receptor, sulfotransferase 1A1 and tumour necrosis factor ligand superfamily member 12 in protecting against AF. Fibroblast growth factor 5, interleukin-2 receptor subunit β, and tumour necrosis factor had a causal effect, increasing AF risk. The mediation exploration indicated that the indirect effect of genus <i>Lachnospiraceae</i> (FCS020 group) (id: 11314) on AF mediated by interleukin-18 was OR 1.015 (95% confidence interval 1.000–1.037; mediation proportion = 9.494%). This study supplies genetic insights into the potential causal association between the gut microbiota and AF. These causal associations and mediating effects are useful for managing AF through manipulation of the gut microbiota.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70379","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143380121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic Potential of Gasdermin D-Mediated Myocardial Pyroptosis in Ischaemic Heart Disease: Expanding the Paradigm From Bench to Clinical Insights","authors":"Chanon Piamsiri,&nbsp;Chayodom Maneechote,&nbsp;Siriporn C. Chattipakorn,&nbsp;Nipon Chattipakorn","doi":"10.1111/jcmm.70357","DOIUrl":"https://doi.org/10.1111/jcmm.70357","url":null,"abstract":"<p>Ischaemic heart disease (IHD) remains a leading cause of global morbidity and mortality. One significant contributor to the pathology of IHD is the excessive release of inflammatory mediators during the disease progression. Pyroptosis is a form of programmed cell death (PCD) triggered by the activation of inflammasomes and caspase 1. The activation of inflammatory caspase 1 proteolytically cleaves gasdermin D (GSDMD) to the activated form amino acid terminus (GSDMD-NT), leading to disruption of the plasma membrane. This cascade of events is considered the canonical pathway of pyroptosis. IHD also caused oxidative stress, thereby triggering noncanonical pyroptosis via the activation of caspases 4/5/11. Previous studies have provided compelling evidence of the close relationship between pyroptosis and the aetiology of IHD (e.g., acute myocardial infarction, myocardial ischaemia and reperfusion injury and chronic myocardial infarction), as well as the association of pyroptosis with unfavourable clinical outcomes. Several interventions aimed at targeting pyroptosis have demonstrated promising therapeutic benefits against IHD-related pathologies. This review provides mechanistic insights into the roles of pyroptosis in IHD from in vitro, in vivo and clinical perspectives. In-depth understanding into this area could also pave the way for the future development of novel therapeutic strategies targeting pyroptosis in IHD.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70357","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143380377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single Cell RNA-Seq Identifies Cell Subpopulations Contributing to Idiopathic Pulmonary Fibrosis in Humans","authors":"Tangjuan Zhang,&nbsp;Zhichao Hou,&nbsp;Zheng Ding,&nbsp;Peng Wang,&nbsp;Xue Pan,&nbsp;Xiangnan Li","doi":"10.1111/jcmm.70402","DOIUrl":"https://doi.org/10.1111/jcmm.70402","url":null,"abstract":"<p>The cell populations, particularly subpopulations, involved in the onset and progression of idiopathic pulmonary fibrosis (IPF) remain incompletely understood. This study employed single-cell RNA-seq to identify cell populations and subpopulations with significantly altered proportions in the lungs of patients with IPF. In IPF lungs, endothelial cell proportions were significantly increased, while alveolar epithelial cell proportions were markedly decreased. Among the three identified fibroblast subpopulations, the proportion of myofibroblasts was significantly increased, while the proportions of the other two fibroblast subtypes were reduced. Similarly, within the three macrophage subpopulations, the macrophage_SPP1 subpopulation, localised to fibroblastic foci, showed a significant increase in proportion, while the alveolar macrophage subpopulation was significantly reduced. Trajectory analysis revealed that fibroblasts in IPF lungs could differentiate into myofibroblasts, and alveolar macrophages could transition into the macrophage_SPP1 subpopulation. Among T-cell subpopulations, only the CD4 T_FOXP3 subpopulation exhibited a significant change, whereas all four B-cell subpopulations showed significant proportional shifts. These findings provide a comprehensive view of the cellular alterations contributing to IPF pathogenesis. Extensive interactions among various cell populations and subpopulations were identified. The proportions of various cell populations and subpopulations in IPF lungs, including endothelial cells, fibroblasts, macrophages and B cells, were significantly altered. Further in-depth investigation into the roles of cell subpopulations with significantly altered proportions in the onset and progression of IPF will provide valuable insights into the pathological mechanisms underlying the disease. This understanding could facilitate the development of novel therapeutic strategies and medications for IPF treatment.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70402","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143380445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}