JOURNAL OF MOLECULAR MEDICINE-JMM分子医学杂志
JOURNAL OF MOLECULAR MEDICINE-JMM(英文缩写 J MOL MED),ISSN 0946-2716,eISSN 1432-1440,中文译名:分子医学杂志 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：2025-09-27 至 2026-09-27，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 | 5.606 | Q1 |
| 2022 | 4.700 | Q1 |
| 2023 | 4.800 | Q1 |
| 2024 | 4.200 | Q1 |
| 2025 | 5.000 | Q1 |
JOURNAL OF MOLECULAR MEDICINE-JMM 最新收录文献
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1. Unravelling deregulated metabolites in seminal plasma of infertile men: a systematic review and bioinformatic analysis.
PMID:日期:2026-09-25Male infertility is a multifactorial condition accounting for 50% of infertility cases. Although conventional semen analysis remains the standard method for male infertility diagnosis, it fails to explain 30% of the cases and their underlying molecular causes. Metabolomics offers valuable insights into sperm metabolic dysfunction, enabling the identification of deregulated pathways involved in male infertility. Here, a systematic review including metabolomic studies that compare the seminal plasma metabolome of healthy and infertile men was conducted. A literature search was conducted in PubMed, Scopus, and Web of Science databases following PRISMA guidelines. Twenty metabolomic studies published until December 2025 were included and categorized into four groups: asthenozoospermia, oligozoospermia, obesity, and overall male infertility. A total of 284 metabolites were retrieved, of which eleven (down: L-tyrosine, D-fructose, L-valine, phenylalanine, proline, D-glucose, L-alanine, leucine, sorbitol, L-aspartic acid; up: uridine), six (down: D-fructose, glycine, maleic acid, L-valine, proline, and lysine), and ten (down: L-carnitine, L-tyrosine, L-valine, L-alanine, phenylalanine, proline, D-glucose, leucine, malic acid, and citraconic acid) were altered in asthenozoospermia, obesity, and overall infertility groups, respectively. These metabolites were associated with phenylalanine/tyrosine metabolism, fructose and mannose degradation, and β-oxidation of long-chain fatty acids. A bioinformatic analysis of the enzymes possibly involved in these pathways revealed associations with male infertility phenotypes and key sperm functions, including motility, vitality, and energy metabolism. This study provides a list of metabolites altered in the seminal fluid of infertile men, highlighting their potential as biomarkers of male infertility, and gives insights into the metabolic pathways affected in these conditions.
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3. MicroRNA-122 as a regulator and biomarker of liver disease.
3. MicroRNA-122作为肝病的调控因子和生物标志物PMID:日期:2026-09-19MicroRNA-122 (miR-122) is the most abundant liver-specific microRNA, comprising ~ 70% of the hepatic miRNA pool, and a central regulator of lipid metabolism, inflammation, fibrosis, viral replication, and hepatocarcinogenesis. This review synthesizes experimental, clinical, and molecular evidence on the role of miR-122 across the spectrum of liver disease, including metabolic dysfunction-associated fatty liver disease (MAFLD) and steatohepatitis (MASH), drug-induced acute liver injury, hepatitis B and C virus (HBV/HCV) infection, hepatocellular carcinoma (HCC), and colorectal cancer liver metastasis. Mechanistically, miR-122 governs hepatic lipogenesis through the Sirt1/LKB1/AMPK axis, modulates inflammation via LPS/TLR-4/FoxO3 signaling, and exerts tumor-suppressive and antiviral effects through Cyclin G1/p53, HO-1, NDRG3, GALNT10, PEG10, and NEGR1. A recurring theme is the compartment- and stage-dependent behavior of miR-122: hepatic expression declines with disease progression, whereas circulating levels rise with hepatocyte injury, reconciling apparently contradictory reports and underscoring the importance of specimen source and disease stage in biomarker interpretation. We further contrast the etiology-specific regulation of miR-122 in HBV- versus HCV-associated disease, in which epigenetic silencing and interferon-linked mechanisms drive divergent expression. Finally, we critically appraise the failed clinical translation of anti-miR-122 therapeutics (miravirsen, RG-101), highlighting viral resistance, safety liabilities, and the tumor-suppressor paradox that constrains inhibition-based strategies. Collectively, miR-122 emerges as a minimally invasive biomarker and a biologically informative, though therapeutically challenging, target in liver disease.
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4. Prospective associations of premature senescence, inflammation, and MERCSs in the cardioprotective effect of CBD in HFpEF.
PMID:日期:2026-09-18Heart failure with preserved ejection fraction (HFpEF) remains a clinical challenge lacking effective therapies. While Cannabidiol (CBD) suggests cardioprotective potential, its efficacy and underlying in HFpEF are poorly understood. This study investigated the effects of CBD on a murine model of HFpEF induced by a high-fat diet and L-NAME for 8 weeks. CBD was administered subcutaneously every three days. Hemodynamic performance was assessed via invasive pressure-volume loops, complemented by histological analysis and oxidative stress markers. Cellular senescence, NLRP3-mediated inflammation and Mitochondria-Endoplasmic Reticulum Contact Sites (MERCSs) were evaluated through immunofluorescence, RT-qPCR, and transmission electron microscopy. CBD treatment failed to reduce cardiac hypertrophy but improves cardiac fibrosis and diastolic dysfunction. These improvements were associated with a marked reduction in senescent cells accumulation and on systemic cytokine levels that may be associated with the senescence-associated secretory phenotype (SASP). Notably, CBD suppressed the NLR3-mediated proinflammatory state by preserving inter-organelle distance and MERCSs integrity. Our findings demonstrate, for the first time, that CBD modulates MERCSs communication to regulate senescence and inflammation in HFpEF. These results position CBD as a promising intervention for mitigating the pathology of HFpEF through the regulation of MERCSs, although the signaling pathways involved in this protective mechanism need to be characterized.
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6. {"_":"METTL3 mitigates age-related hearing loss by inhibiting NF-κB-mediated inflammatory responses through the mA modification of NFKBIA.","sup":["6"]}
PMID:日期:2026-09-18Age-related hearing loss (ARHL) is a prevalent and debilitating sensory deficit in the elderly, with chronic inflammation being a key pathogenic driver. The RNA methyltransferase METTL3, a primary mediator of N6-methyladenosine (m6A) modification, has been implicated in various aging-related diseases; however, its functional role and mechanism in ARHL remain poorly defined. ARHL models were established using 12-month-old C57BL/6 mice and by treating HEI-OC1 auditory cells with LPS and D-galactose. Auditory function and cochlear pathology were assessed through auditory brainstem response (ABR) thresholds and hematoxylin-eosin (H&E) staining, respectively. Inflammatory cytokine levels, gene and protein expression, were measured using ELISA, qPCR, Western blotting, and immunofluorescence. The molecular mechanism of METTL3 in inflammation was investigated using m6A RNA methylation quantification kit, RIP-qPCR analysis, and RNA stability assay. We found that both NFKBIA and METTL3 were significantly downregulated in the cochleae of ARHL mice. In HEI-OC1 cells, overexpression of NFKBIA suppressed the NLRP3 inflammasome and the pro-inflammatory NF-κB/IL-6/STAT3 axis. Furthermore, METTL3 overexpression mitigated NF-κB-mediated inflammation, an effect that was significantly attenuated upon NFKBIA knockdown. Mechanistically, METTL3 directly bound to NFKBIA mRNA and enhanced its stability through m6A modification. Critically, in ARHL mice, METTL3 overexpression restored NFKBIA levels, ameliorated hearing loss and cochlear damage, and suppressed the activation of the NLRP3 inflammasome and the NF-κB/IL-6/STAT3 pathway. Collectively, METTL3 mitigated ARHL by downregulating the NF-κB/IL-6/STAT3/NLRP3-mediated inflammatory responses through the enhancement of NFKBIA m6A modification.
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8. Anti-hyperuricemia therapy alleviates diet-induced gut inflammation via AhR-IL-22-signalling.
PMID:日期:2026-09-04High-fat diets (HFD) are implicated in metabolic disorders through mechanisms involving hyperuricemia, gut dysbiosis, and intestinal barrier dysfunction. This study investigated the effects of pharmacological uric acid reduction on gut homeostasis in HFD-fed mice. We assessed serum uric acid, gut microbial composition, pro- and anti-inflammatory cytokine expression, intestinal barrier dysfunction markers, and tryptophan metabolism in mice subjected to HFD with or without allopurinol treatment. AhR antagonist CH-223191 was used to provide functional evidence for the role of AhR activation in mediating the observed effects. HFD induced hyperuricemia, microbial dysbiosis characterized by increased Proteobacteria and altered Firmicutes/Bacteroidetes ratios, and elevated pro-inflammatory cytokines (IL-1β, IL-6, TNF-α). These changes correlated with decreased IL-10 and IL-22, increased serum LPS, and systemic inflammation (IL-6, CRP). Allopurinol treatment normalized uric acid levels, restored microbial balance, reduced gut and systemic inflammation, improved intestinal barrier function, and modulated tryptophan metabolism by decreasing IDO1 activity and restoring indole production. Pharmacological blockade of AhR with CH-223191 reversed the anti-inflammatory and barrier-protective effects of allopurinol treatment, providing functional evidence for the role of AhR/IL22 axis in mediating gut protection. Targeting hyperuricemia effectively reverses HFD-induced gut dysbiosis, inflammation, and barrier dysfunction through metabolite-mediated immunoregulatory mechanisms involving the AhR-IL-22 axis. These findings propose uric acid modulation as a promising therapeutic strategy for metabolic and inflammatory gut diseases.
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9. Neutrophil extracellular traps in tumor progression: from mechanistic insights and regulatory factors to clinical detection and diagnosis.
PMID:日期:2026-09-01Neutrophil extracellular traps (NETs), web-like DNA structures released by neutrophils, were initially recognized as key components of the anti-infective immune response but are now implicated in tumor progression. Tumor cells orchestrate the reprogramming of tumor-associated neutrophils (TANs) and trigger NET formation through paracrine signaling, thereby establishing a "tumor cell-TAN-NETs" positive feedback loop. This axis serves not only as a key hub for awakening dormant tumor foci and mediating immune evasion, but also as a core mechanism driving distant metastasis and dictating poor clinical prognosis. Notably, targeted disruption of this axis effectively reverses tumor therapy resistance and significantly sensitizes tumors to radiotherapy, chemotherapy, and immune checkpoint blockade, establishing NETs as novel therapeutic targets poised to overcome the current bottlenecks in cancer treatment. Nevertheless, limitations in detection technologies, prognostic modeling challenges, tumor heterogeneity, and inconsistent research findings constrain clinical translation. Future studies should prioritize optimizing detection methods, conducting rigorous clinical validation, and identifying specific therapeutic targets to accelerate the translational progress of NETs from basic research to clinical practice. This review synthesizes current knowledge on the biological mechanisms, regulatory pathways, and detection approaches of NETs, providing a theoretical basis for their clinical application in precision oncology.
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10. SREBF2 promotes mitophagy and protects against ferroptosis via Cav-1-regulated PINK1/Parkin signaling in ischemic heart failure.
10. SREBF2通过Cav-1调控的PINK1/Parkin信号通路促进线粒体自噬并防止铁死亡，在缺血性心力衰竭中发挥保护作用PMID:日期:2026-08-27Myocardial infarction-induced heart failure (MI-HF) remains a major contributor to cardiovascular mortality, yet the molecular mechanisms underlying its progression, particularly those involving ferroptosis, are not fully understood. This study aimed to investigate the role of SREBF2 in regulating ferroptosis and mitochondrial homeostasis in MI-HF. Differentially expressed genes were screened from the GSE24519 dataset and overlapped with ferroptosis-related genes, identifying SREBF2 as a potential target. SREBF2 expression was examined in human HF samples, MI-HF mice, and oxygen-glucose deprivation (OGD)-injured cardiomyocytes. Functional roles of SREBF2 were evaluated through in vivo overexpression in mice and in vitro assays in cardiomyocytes. Ferroptosis markers (GPX4, ACSL4, ROS, MDA, Fe²⁺, GSH), mitochondrial membrane potential (ΔΨm), and mitophagy-related proteins (PINK1, Parkin, p62) were assessed. Chromatin immunoprecipitation and rescue experiments were conducted to confirm the transcriptional regulation of Caveolin-1 (Cav-1) by SREBF2. SREBF2 was significantly downregulated in MI-HF tissues and OGD-injured cardiomyocytes. Overexpression of SREBF2 improved cardiac function, reduced infarct size and fibrosis, and enhanced myocardial remodeling in MI-HF mice. SREBF2 suppressed ferroptosis by reducing ROS, Fe²⁺, and MDA levels, restoring GSH and GPX4, and downregulating ACSL4. Mitochondrial dysfunction was alleviated via improved ΔΨm, reduced mitoROS, and balanced mitochondrial dynamics. SREBF2 activated PINK1/Parkin-mediated mitophagy, which was essential for its anti-ferroptotic effects. Mechanistically, SREBF2 directly bound to and transcriptionally activated Cav-1, which mediated downstream mitophagy activation and ferroptosis inhibition. Cav-1 knockdown or mitophagy inhibition abrogated SREBF2-induced mitochondrial protection and cytoprotection. The results of our study demonstrate that SREBF2 mitigates MI-induced HF by activating the Cav-1/PINK1/Parkin axis to promote mitophagy and inhibit ferroptosis. These findings reveal a novel cardioprotective mechanism and identify SREBF2 as a promising therapeutic target in heart failure.