JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY分子与细胞心脏病学杂志
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY(英文缩写 J MOL CELL CARDIOL),ISSN 0022-2828,eISSN 1095-8584,中文译名:分子与细胞心脏病学杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 5.763 | Q2 |
| 2022 | 5.000 | Q2 |
| 2023 | 4.900 | Q1 |
| 2024 | 4.700 | Q1 |
| 2025 | 4.900 | Q1 |
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY 最新收录文献
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1. Multi-omic analysis reveals maturation programs in human pluripotent stem cell-derived cardiomyocytes during long-term culture.
PMID:日期:2026-10-02Human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) hold tremendous promise for disease modeling, drug discovery, and cardiac regenerative therapies. However, the immature phenotype of hPSC-CMs remains a major barrier limiting their translational utility. Here, we performed integrated multi-omic profiling to identify molecular pathways and regulatory programs associated with hPSC-CM maturation during long-term culture. hPSC-CMs were cultured for 113 days and analyzed using metabolomics, proteomics, and transcriptomics across progressive stages of maturation. Long-term culture induced widespread multi-omic remodeling, including significant changes in 142/934 metabolites, 550/3556 proteins, and 2892/23,309 transcripts from Day 30 to Day 113. Metabolomic analyses revealed early increases in phospholipid biosynthesis and mitochondrial beta oxidation of fatty acids from Day 30 to Day 60, suggesting metabolic priming precedes later maturation events. In contrast, proteomic remodeling was more prominent during later stages of maturation and was characterized by enhanced calcium handling and cell cycle exit. Transcriptomic analyses demonstrated progressive increases in ion channel expression, t-tubule organization, fatty acid metabolism, creatine shuttle pathways, and cell cycle arrest programs. Transcriptomic and integrative multi-omic pathway analyses identified coordinated suppression of TGFβ, MAPK, Wnt, and Hedgehog signaling together with activation of integrin-related, respiratory electron transport, muscle contraction, and Slit-Robo signaling pathways during maturation. Moreover, multi-omic transcription factor activity analysis prioritized a GATA4-centered network of putative cardiomyocyte maturation regulators including SOX7, SOX18, TBX2, and ZFPM2 (FOG2). Together, these findings elucidate the degree and pace of hPSC-CM maturation during long-term culture and establish an integrated multi-omic framework for identifying strategies to accelerate hPSC-CM maturation.
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2. Myocardial mitochondrial morphology and oxidative phosphorylation capacity in wild-type transthyretin amyloid cardiomyopathy.
2. 野生型转甲状腺素蛋白淀粉样变心肌病中的心肌线粒体形态与氧化磷酸化能力PMID:日期:2026-09-26The effects of amyloid deposition on myocyte mitochondrial morphology and oxidative function in wild-type transthyretin cardiac amyloidosis (ATTRwt) are poorly understood. Endomyocardial biopsies of patients with ATTRwt were investigated with electron microscopy to determine mitochondrial structure, numbers, and size. High-resolution respirometry was used to determine mitochondrial oxidative phosphorylation. Amyloid load was assessed using both the stereological counting method, cardiac resonance imaging, and echocardiography. Regression analysis was performed to assess associations between amyloid load variables and oxidative phosphorylation capacity. In 52 patients with ATTRwt, the proportion of morphologically normal mitochondria was 48% [30-74], and the oxidative phosphorylation capacity was 84.2 ± 30.1 pmol O2/(mg*s). The mitochondrial area was significantly associated with mitochondrial oxidative phosphorylation capacity (Estimate 289 [CI95: 52-526, p = 0.02] per 1 um2 area). Stratification by median echocardiography structural variables demonstrated significantly lower mitochondrial numbers, size, and oxidative function with increased wall thickness. Stratification by cardiac magnetic resonance-derived extracellular volume (n = 32) and stereology-derived amyloid load (n = 29) medians demonstrated no significant differences in numbers, morphology, or function. Regression analysis found no significant associations between amyloid load variables and oxidative phosphorylation capacity. Cardiac mitochondrial structure is affected, and oxidative phosphorylation capacity is low in ATTRwt. Echocardiography grouping was able to demonstrate differences in mitochondrial numbers, size, and oxidative function with increasing wall thickness. Regression analysis was unable to demonstrate significant associations between measures of amyloid load and mitochondrial oxidative phosphorylation capacity.
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3. Graft IL-33/ST2 signaling promotes cardiac allograft vasculopathy by modulating cardiac resident cell function.
PMID:日期:2026-09-11Chronic rejection and subsequent cardiac allograft vasculopathy (CAV) remain critical challenges in transplantation. Although IL-33/ST2 signaling has been implicated in CAV progression, its precise cellular and molecular mechanisms, particularly its regulation of cardiac resident cells, remain incompletely understood. In this study, we demonstrated that graft-specific ST2 deficiency significantly attenuated allograft vasculopathy, reduced immune cell infiltration, and mitigated fibrosis. RNA sequencing revealed decreased expression of genes associated with transplant rejection, adhesion molecules and chemokines in ST2-deficient allografts. Mechanistically, IL-33 directly activated cardiac-resident endothelial cells (ECs), smooth muscle cells (SMCs), and fibroblasts, driving their proliferation, dysfunction, and aberrant release of proinflammatory and profibrotic cytokines. Importantly, graft ST2 deficiency selectively attenuated the stimulating effect IL-33 on these resident cells while preserving its regulatory functions in other cell types, particularly recipient immune cells, thus reducing chronic rejection and CAV. Our findings elucidate a pivotal role for graft-specific IL-33/ST2 signaling in CAV pathogenesis and highlight its therapeutic potential as a targeted intervention.
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4. Mitofusin 2 deficiency causes atrial lipid accumulation in experimental and human atrial fibrillation and diabetes mellitus.
PMID:日期:2026-09-09Atrial fibrillation (AF) is the most common tachyarrhythmia, with diabetes mellitus (DM) as a key risk factor. DM is linked to cardiac lipid toxicity. We previously found that the mitochondrial outer membrane protein Mitofusin 2 (MFN2) is reduced in AF and further suppressed in DM. However, whether MFN2 contributes to altered lipid metabolism remains unclear. Atrial tissue from diabetic (db/db) and wild-type mice and atrial appendages from patients with AF or sinus rhythm were analyzed. AF- and DM-like conditions were modeled in human, rat, and mouse atrial myocytes using tachypacing (TP) and high glucose (HG). MFN2 expression was modulated by siRNA knockdown or plasmid-based overexpression. Lipid droplets (LDs), intracellular fatty acid distribution, LD-mitochondria colocalization, carnitine-dependent fatty acid metabolic activity, and mitochondrial respiration were assessed. DM model db/db mice and AF patients exhibited reduced MFN2 expression and increased LD accumulation. Similarly, TP and HG treatments reduced MFN2 levels, increased LD content, and decreased LD-mitochondria colocalization in atrial myocytes across species. MFN2 knockdown increased LD accumulation, whereas MFN2 overexpression attenuated lipid accumulation under basal and stress conditions. Functionally, MFN2 reduction was associated with decreased FAO capacity and redistribution of fatty acids toward lipid droplets and away from mitochondria. These effects were not observed with MFN1 manipulation, suggesting isoform-specific regulation. MFN2 regulates atrial lipid metabolism and is associated with lipid accumulation and altered lipid droplet-mitochondria organization in AF and DM. These findings identify a potential link between mitochondrial dynamics and lipid metabolic remodeling in atrial disease.
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5. PP2A promotes myocardial regeneration through YAP.
5. PP2A通过YAP促进心肌再生PMID:日期:2026-09-09该文献暂无摘要。
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6. Pharmacological modulation of GLI signaling promotes human iPSC-derived cardiomyocyte maturation via PGC1α-associated mitochondrial programs.
6. GLI信号的药理学调控通过PGC1α相关的线粒体程序促进人iPSC来源的心肌细胞成熟PMID:日期:2026-09-09Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) provide a scalable platform for cardiovascular research but remain structurally and functionally immature, limiting their utility for studying cardiac biology, disease mechanisms, and clinical translation. Developmental signaling pathways that coordinate cardiomyocyte maturation remain incompletely understood. Here, we investigated whether pharmacological modulation of GLI signaling promotes a shift toward a more mature hiPSC-CM phenotype through PGC1α-linked mitochondrial and metabolic programs using both 2D and 3D engineered models. Treatment of hiPSC-CMs with GANT61 led to coordinated changes consistent with relative cardiomyocyte maturation, including increased cellular anisotropy, improved sarcomeric organization, reduced spontaneous beating rate, and advanced action potential characteristics. In contrast, pharmacological or genetic activation of GLI signaling suppressed maturation-associated phenotypes. In 3D-engineered heart tissues (EHTs), GLI modulation improved cellular alignment, tissue organization and contractile function. Transcriptomic and gene expression analyses revealed enrichment of mitochondrial and metabolic pathways, including increased expression of PGC1α, NRF1, and MFN2, together with upregulation of fatty acid oxidation-related gene programs. Confocal imaging demonstrated more extensive mitochondrial networks with increased branching and connectivity. Supporting these findings, we found elevated mtND1 and mtND5 levels, consistent with increased mitochondrial DNA copy number and mitochondrial biogenesis. Mechanistically, GANT61 increased MEF2A transcripts with a concomitant induction in protein levels, and motif analysis identified MEF2A binding sites in the proximal PGC1α promoter, suggesting a putative role for MEF2A in mediating PGC1α expression. Furthermore, pharmacological inhibition of PGC1α attenuated GANT61-induced structural and functional changes, supporting a PGC1α-dependent mechanism. Collectively, these findings identify GLI signaling as a modulatory pathway influencing the structural, electrophysiological, and mitochondrial gene programs associated with hiPSC-CM maturation and highlight GLI modulation as a strategy to enhance the physiological relevance of hiPSC-derived cardiac models.
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7. Whole-genome sequencing identifies a c.1282C > T missense variant in Taurine Transporter (TauT) associated with taurine-mediated dilated cardiomyopathy in a family of domestic shorthair cats.
7. 全基因组测序在一个家养短毛猫家系中鉴定出牛磺酸转运体（TauT）的c.1282C > T错义变异，该变异与牛磺酸介导的扩张型心肌病相关PMID:日期:2026-09-09Taurine is a cytoprotectant amino acid critical for a variety of cellular functions, including cell volume and intracellular calcium regulation, bile salt formation, free radical protection, and mitochondrial biogenesis. In most mammals, taurine is synthesized via methionine transsulfuration; albeit, in cats, taurine biosynthesis is blunted due to low enzymatic activity of their encoded cysteine sulfonic acid decarboxylase and, therefore, is an essential amino acid in the species. Taurine deficiency in cats results in retinopathy, coagulopathy, growth retardation, impaired immunological function, and most notably dilated cardiomyopathy (DCM). A three-year-old domestic shorthair cat was evaluated for vomiting, anorexia, and lethargy. Severe dilated cardiomyopathy and taurine deficiency were identified, despite eating a commercial, nutritionally balanced, diet with adequate taurine concentrations. A whole-genome association study (WGAS), under the assumptions of an incomplete dominance mode of inheritance (MOI), was performed on this case and two related cats with mild taurine and echocardiographic abnormalities (i.e., queen and littermate) compared to 18 previously whole-genome sequenced echocardiographically-normal geriatric controls (>10 years-of-age; n = 21). A 'MODERATE' c.1282C > T; p.Arg428Trp variant harbored in Solute Carrier Family 6 Member 6/Taurine Transporter (SLC6A6/TauT) was identified. The variant segregated to the postulated MOI and was not observed in any of the control or in an expanded population of cats (n = 422). Functional analyses involving wildtype and mutant SLC6A6 overexpression in HEK293-derived cells revealed marked reduction in cellular taurine uptake and decreased plasma membrane expression in those harboring the c.1282C > T variant. This represents the first-ever reported genetic variant explaining taurine deficiency in any domestic animal species.
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8. {"_":"Icosapent ethyl activates GPR120 to improve post-myocardial infarction cardiac remodeling by suppressing CXCR3 inflammatory cells.","sup":["+"]}
8. 二十碳五烯酸乙酯激活GPR120，通过抑制CXCR3炎症细胞改善心肌梗死后心脏重构。+PMID:日期:2026-08-22Icosapent ethyl, a high-purity ethyl ester of eicosapentaenoic acid (EPA), has demonstrated cardiovascular benefit in clinical trials; however, its effects on post-myocardial infarction (MI) cardiac remodeling and the underlying cellular mechanisms remain incompletely understood. Here, we investigated the role of icosapent ethyl in regulating post-MI remodeling using a murine MI model with myeloid-specific deletion of the omega-3 fatty acid receptor GPR120. Icosapent ethyl treatment significantly improved survival, preserved left ventricular systolic function, attenuated adverse ventricular remodeling and interstitial fibrosis, reduced cardiomyocyte apoptosis, and preserved myocardial microvascular density after MI. The protective effects of icosapent ethyl were markedly attenuated in myeloid GPR120-deficient mice. Mechanistically, icosapent ethyl activated GPR120 signaling in myeloid cells, suppressed CXCL10 expression, and reduced recruitment of proinflammatory CXCR3 leukocytes into the infarcted myocardium. Pharmacological inhibition of CXCR3 rescued adverse cardiac remodeling in myeloid GPR120-deficient mice, supporting a functional link between myeloid GPR120 activation and CXCR3-dependent inflammatory responses. These findings identify the myeloid GPR120-CXCL10/CXCR3 signaling axis as a critical immunomodulatory pathway by which icosapent ethyl improves post-MI cardiac remodeling, highlighting therapeutic potential of icosapent ethyl to limit inflammation-driven cardiac dysfunction after ischemic injury.
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9. Novel Wnt potentiators induce iPSC-derived cardiomyocyte proliferation and increase embryonic zebrafish heart size.
9. 新型Wnt增强剂诱导iPSC来源的心肌细胞增殖并增加胚胎斑马鱼心脏大小PMID:日期:2026-08-21Canonical Wnt/β-catenin pathway activation can promote cardiomyocyte (CM) cell cycle activity, but translation is limited by off-target and functional liabilities associated with global pathway activation. We identified two small molecules, LRN9 and DF6, which potentiate Wnt/β-catenin signaling through a non-GSK3β mechanism and induce CM cell-cycle re-entry in human iPSC-CMs. In cardiac organoids, the effects was largely restricted to CMs and were accompanied by minimal changes in contractile and relaxation parameters, in contrast to reported impairment with GSK3β inhibition. RNA-sequencing showed enrichment of DNA replication and cell-cycle pathways. In embryonic zebrafish, both compounds increased ventricular growth consistent with CM hyperplasia.
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10. Site-specific O-GlcNAcylation of Nrf2 regulates myocardial ischemia-reperfusion injury.
10. Nrf2的特定位点O-GlcNAc糖基化调节心肌缺血再灌注损伤PMID:日期:2026-08-20Myocardial ischemia/reperfusion (I/R) injury is a major cause of morbidity and mortality. Although both nuclear factor erythroid 2-related factor 2 (Nrf2) and O-GlcNAcylation play critical protective roles in myocardial I/R injury, it remains unclear the role of Nrf2 O-GlcNAcylation in cardiac injury following I/R. An in vivo I/R model in mice and an in vitro oxygen-glucose deprivation/reperfusion (OGD/R) model in AC16 cardiomyocytes were employed. Histology, serum markers, and oxidative stress assays were used to assess injury. Site-directed mutagenesis, co-immunoprecipitation, western blot, and qPCR were utilized to identify O-GlcNAcylation sites and investigate the functional consequences of Nrf2 mutations (S215A and S33A) on its localization, transcriptional activity, and cell injury. Nrf2 underwent time-dependent O-GlcNAcylation following myocardial I/R injury in vivo and in vitro. During the early phase (6 h) of OGD/R, O-GlcNAcylation at Ser215 promoted Nrf2 nuclear translocation, activated the expression of antioxidant genes (HO-1, NQO1, and SOD2), and conferred cyto-protection in AC16 cardiomyocytes. In contrast, during the later phase (24 h), O-GlcNAcylation at Ser33 inhibited Nrf2 nuclear accumulation, suppressed its transcriptional activity, and exacerbated oxidative injury. The S215A mutation abolished the early protective effects, whereas the S33A mutation significantly attenuated the late-phase damage. This study identified a novel O-GlcNAcylation switch at Nrf2 Ser215 and Ser33 that governs the shift from protection to injury in the myocardium following I/R, highlighting the therapeutic potential of site-specific O-GlcNAcylation for cardioprotection.