Journal of cellular biochemistry最新文献_第3页

Notoginsenoside R1 Alleviates Macrophage Inflammatory Responses via Modulating the JAK1/STAT3 Pathway 三七皂苷R1通过调控JAK1/STAT3通路缓解巨噬细胞炎症反应

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-07-29 DOI: 10.1002/jcb.70112

Chengjie Wu, Shuting Hou, Meizhi Liu, Hualin Feng, Xu Jiang, Nengneng Ji, Fang Fang

{"title":"Notoginsenoside R1 Alleviates Macrophage Inflammatory Responses via Modulating the JAK1/STAT3 Pathway","authors":"Chengjie Wu, Shuting Hou, Meizhi Liu, Hualin Feng, Xu Jiang, Nengneng Ji, Fang Fang","doi":"10.1002/jcb.70112","DOIUrl":"10.1002/jcb.70112","url":null,"abstract":"<div>\u0000 \u0000 <p>Notoginsenoside R1 (NR1), an active component of <i>Panax notoginseng</i>, may exert anti-atherosclerotic effects by modulating macrophage M1/M2 polarization. This study aimed to investigate the specific mechanism of NR1 against atherosclerosis based on the JAK1/STAT3 pathway. M1 and M2 macrophage models, as well as an ox-LDL-induced macrophage model, were established. These models were treated with varying concentrations of NR1. Our results demonstrated that NR1 effectively suppressed LPS/IFN-γ or ox-LDL-induced polarization of macrophages toward the pro-inflammatory M1 phenotype and promoted their transition to the anti-inflammatory M2 phenotype. Concurrently, NR1 significantly inhibited the phagocytosis of ox-LDL by macrophages in the atherosclerosis model, reduced lipid accumulation, and improved mitochondrial function. Mechanistically, the regulatory effects of NR1 on macrophage polarization and function primarily depended on the inhibition of the JAK1/STAT3 signaling pathway. In conclusion, this study suggests that NR1 targets the JAK1/STAT3 pathway to balance macrophage M1/M2 polarization, thereby suppressing inflammatory responses, and ultimately alleviating atherosclerosis.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"127 8","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148603340","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}

引用次数: 0

Novel Endocrine Signaling Axis in Cardiovascular-Kidney-Metabolic Syndrome: Interactions and Therapeutic Potential of FGF21 and GDF15 心血管-肾-代谢综合征的新型内分泌信号轴：FGF21和GDF15的相互作用和治疗潜力。

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-07-28 DOI: 10.1002/jcb.70113

Changlong Yang, Lei Chen, Hong Xiao, Wanghang Wei, Jiafei Liang, Tao Chen, Tao Yang, Yi Ma

{"title":"Novel Endocrine Signaling Axis in Cardiovascular-Kidney-Metabolic Syndrome: Interactions and Therapeutic Potential of FGF21 and GDF15","authors":"Changlong Yang, Lei Chen, Hong Xiao, Wanghang Wei, Jiafei Liang, Tao Chen, Tao Yang, Yi Ma","doi":"10.1002/jcb.70113","DOIUrl":"10.1002/jcb.70113","url":null,"abstract":"<div>\u0000 \u0000 <p>Cardiovascular-Kidney-Metabolic Syndrome (CKM) is a multisystem disorder characterized by interdependent cardiovascular, renal, and metabolic dysfunction. It commonly involves metabolic conditions such as type 2 diabetes and obesity and is associated with substantial morbidity and mortality Recently, stress-induced hormone-like cytokines, fibroblast growth factor 21 (FGF21) and growth differentiation factor 15 (GDF15), are emerging as the central two-controllers of the pathophysiological network of CKM. This review is a systemic summary of the biological functions and mechanism of interaction between FGF21 and GDF15 in CKM with a focus on the functions of these two hormones in regulating energy metabolism, insulin sensitivity, inflammation, fibrosis, and cardiovascular protection. We examine their clinical relevance as disease biomarkers and discuss their prospective potential as newer therapeutic targets, in addition to discussing the obstacles that are still in the way of our translations of these findings into therapeutic application. This article will elucidate shared and distinct actions of FGF21 and GDF15 and thereby offer a thorough comprehension of integrative endocrine signaling axis output, as well as its implication to further the development of CKM management.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"127 8","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148603332","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}

引用次数: 0

EXPRESSION OF CONCERN: Downregulation of the Upstream Binding Factor1 by Glycogen Synthase Kinase3β in Myeloid Cells Induced to Differentiate 关注的表达：糖原合成酶激酶3β在诱导分化的髓细胞中下调上游结合因子1

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-07-17 DOI: 10.1002/jcb.70102

{"title":"EXPRESSION OF CONCERN: Downregulation of the Upstream Binding Factor1 by Glycogen Synthase Kinase3β in Myeloid Cells Induced to Differentiate","authors":"","doi":"10.1002/jcb.70102","DOIUrl":"https://doi.org/10.1002/jcb.70102","url":null,"abstract":"<p><b>EXPRESSION OF CONCERN</b>: M. Liu, X. Tu, G. Ferrari-Amorotti, B. Calabretta, and R. Baserga, “Downregulation of the Upstream Binding Factor1 by Glycogen Synthase Kinase3β in Myeloid Cells Induced to Differentiate,” <i>Journal of Cellular Biochemistry</i> 100, no. 5 (2007): 1154–1169, https://doi.org/10.1002/jcb.21103.</p><p>This Expression of Concern is for the above article, published online on 24 October 2006 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Lucie Kalvodova; and Wiley Periodicals LLC. The Expression of Concern has been agreed due to concerns raised by third parties. Specifically, anomalies have been detected in the C/EBP-ER blot presented in Figure 9A including band duplication affecting lanes 5 and 6, and 8 and 9, as well as the total absence of background signal in lanes 1–4. The authors could not be reached for comment; the corresponding author has been reported deceased in the literature. Therefore, the journal has decided to issue an Expression of Concern to inform and alert the readers.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"127 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70102","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467168","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}

引用次数: 0

RETRACTION: Neuroprotective Effect of Licochalcone a Against Oxygen-glucose Deprivation/Reperfusion in Rat Primary Cortical Neurons by Attenuating Oxidative Stress Injury and Inflammatory Response via the SIRT1/Nrf2 Pathway 回缩：甘草查尔酮a通过SIRT1/Nrf2通路减轻氧化应激损伤和炎症反应，对大鼠初级皮质神经元氧糖剥夺/再灌注的神经保护作用

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-07-17 DOI: 10.1002/jcb.70100

{"title":"RETRACTION: Neuroprotective Effect of Licochalcone a Against Oxygen-glucose Deprivation/Reperfusion in Rat Primary Cortical Neurons by Attenuating Oxidative Stress Injury and Inflammatory Response via the SIRT1/Nrf2 Pathway","authors":"","doi":"10.1002/jcb.70100","DOIUrl":"https://doi.org/10.1002/jcb.70100","url":null,"abstract":"<p><b>RETRACTION</b>: X. Liu, Y. Ma, X. Wei, and T. Fan, “Neuroprotective Effect of Licochalcone a Against Oxygen-glucose Deprivation/Reperfusion in Rat Primary Cortical Neurons by Attenuating Oxidative Stress Injury and Inflammatory Response via the SIRT1/Nrf2 Pathway,” <i>Journal of Cellular Biochemistry</i> 119, no. 4 (2018): 3210–3219, https://doi.org/10.1002/jcb.26477.</p><p>The above article, published online on 6 November 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Lucie Kalvodova; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Specifically, multiple image elements in Figure 1 were found to have been previously published in several articles from different author groups and presented in different scientific contexts. The authors did not respond to our requests for clarification. Accordingly, the article has been retracted as the editors consider its conclusions to be invalid. The authors have been informed of the retraction decision but were not available for final confirmation.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"127 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70100","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467169","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}

引用次数: 0

Glucose Metabolism in Immune Regulation: From Mechanisms to Therapeutic Opportunities 免疫调节中的葡萄糖代谢：从机制到治疗机会

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-07-17 DOI: 10.1002/jcb.70111

Takhellambam Malemnganba, Anurag Kumar Pandey, Sramona Kar, Vijay Kumar Prajapati

{"title":"Glucose Metabolism in Immune Regulation: From Mechanisms to Therapeutic Opportunities","authors":"Takhellambam Malemnganba, Anurag Kumar Pandey, Sramona Kar, Vijay Kumar Prajapati","doi":"10.1002/jcb.70111","DOIUrl":"https://doi.org/10.1002/jcb.70111","url":null,"abstract":"<div>\u0000 \u0000 <p>Immune cell activation and differentiation are tightly coupled to metabolic reprogramming, with glucose availability and intracellular glycolytic flux serving as central determinants of immune cell fate and function. While increased glucose uptake and aerobic glycolysis support rapid proliferation and effector programs, persistent glucose abundance or dysregulated glycolytic signaling can contribute to immune dysfunction, chronic inflammation, and impaired host defense. Conversely, controlled limitation of glucose availability—through altered systemic supply, tissue microenvironmental competition, or targeted modulation of glycolysis—can rebalance immune metabolism toward oxidative phosphorylation, fatty acid oxidation, and mitochondrial fitness. This review examines how glucose availability and glycolytic flux operate as metabolic checkpoints that integrate with nutrient-sensing pathways, including mTORC1, AMPK, and HIF-1α, to shape immune activation, effector differentiation, and memory formation. We discuss evidence across disease contexts, including hyperglycemia-associated immune dysfunction, viral infection, autoimmunity, and cancer, and summarize emerging strategies to therapeutically modulate glucose metabolism using dietary interventions and pharmacologic tools. By distinguishing dietary carbohydrate intake from systemic glucose availability and cell-intrinsic glycolytic control, this review provides a coherent framework for understanding when glucose modulation can enhance immunity and when it risks immune suppression or metabolic exhaustion.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"127 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467214","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}

引用次数: 0

Cover Image, Volume 127, Number 7, July 2026 封面图片，127卷，第7期，2026年7月

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-07-15 DOI: 10.1002/jcb.70110

引用次数: 0

Therapeutic Effect of Parthenolide on Paclitaxel-Induced Cardiotoxicity in Rats Parthenolide对紫杉醇所致大鼠心脏毒性的治疗作用。

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-07-12 DOI: 10.1002/jcb.70106

Ufuk Kuşkun, Emine Toraman, Enver Fehim Koçpınar, Mustafa Özkaraca, Hasan Sevgili, Harun Budak

{"title":"Therapeutic Effect of Parthenolide on Paclitaxel-Induced Cardiotoxicity in Rats","authors":"Ufuk Kuşkun, Emine Toraman, Enver Fehim Koçpınar, Mustafa Özkaraca, Hasan Sevgili, Harun Budak","doi":"10.1002/jcb.70106","DOIUrl":"10.1002/jcb.70106","url":null,"abstract":"<div>\u0000 \u0000 <p>The aim of this study was to investigate the therapeutic effects of parthenolide (PTL), the active constituent of <i>Tanacetum parthenium</i>, on paclitaxel (PTX)-induced cardiotoxicity at both gene and protein expression levels. 48 male Sprague-Dawley rats were divided into 6 groups. While no intervention was performed in the control group, the second group received 8 mg/kg PTX. The third group was administered dimethyl sulfoxide (DMSO) as the vehicle control, whereas the fourth, fifth, and sixth groups were treated with 1, 2, and 4 mg/kg PTL, respectively, following PTX administration. The results demonstrated that oxidative stress biomarkers, including glutathione (GSH) and malondialdehyde (MDA), were significantly altered following PTX treatment, indicating oxidative damage; however, PTL administration restored these levels to physiological ranges. Histopathological analyses revealed that PTX caused pathological alterations in cardiac tissue, such as hemorrhage and mononuclear cell infiltration, whereas PTL treatment substantially ameliorated these histopathological lesions. Additionally, 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels, indicative of DNA damage, as well as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) levels, markers of inflammation, were significantly elevated following PTX treatment. PTL administration mitigated these changes, bringing biomarker levels closer to normal. Furthermore, antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPX), and glutathione S-transferase (GST) were assessed at gene expression, enzymatic activity, and protein expression levels. The findings indicate that PTL exerts a potent therapeutic effect against PTX-induced cardiotoxicity. These results support the cardioprotective potential of PTL, suggesting that it mitigates PTX-induced oxidative stress and inflammatory responses.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"127 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148421173","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}

引用次数: 0

Polyethylene Glycol Mediated Inhibition of α-Lactalbumin Aggregation: Molecular Insights From a Carbohydrate-Mimicking Stealth Polymer 聚乙二醇介导的α-乳清蛋白聚集抑制：来自碳水化合物模拟隐形聚合物的分子见解。

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-07-11 DOI: 10.1002/jcb.70107

Priyanka Mudad, Danish Alam, Mohammad Shahid, Arun S. Kharat, Asimul Islam

{"title":"Polyethylene Glycol Mediated Inhibition of α-Lactalbumin Aggregation: Molecular Insights From a Carbohydrate-Mimicking Stealth Polymer","authors":"Priyanka Mudad, Danish Alam, Mohammad Shahid, Arun S. Kharat, Asimul Islam","doi":"10.1002/jcb.70107","DOIUrl":"10.1002/jcb.70107","url":null,"abstract":"<div>\u0000 \u0000 <p>Polyethylene glycols (PEG)-assisted strategies for the development of functionalized and compatible carbohydrate polymers are always an exciting topic for polymer research. However, PEGs, a carbohydrate-mimicking stealth polymer, act as a macromolecular crowding agent that has a significant impact on protein aggregation depending on their concentration and molecular weight. The study systematically investigated the impact of PEG molecules with different molecular weights and concentrations on the thermal aggregation of α-Lactalbumin (α-LA). As the concentration was increased from 10 to 200 mg/mL of each PEG molecule (PEG6000, PEG10000, and PEG20000), the β-sheet aggregates and surface hydrophobicity progressively decreased, indicating the aggregation prevention. Spectroscopic and microscopic results showed that PEGs stabilize α-LA toward its native conformation, indicating the modulation of the protein surface. PEG10000 effectively showed its protective role even at its lowest concentration (10 mg/mL), suggesting its potential role in preserving protein stability and functionality. Thus, this study provides potential therapeutics and industrial applications for the prevention of protein aggregation in different environments.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"127 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148421158","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}

引用次数: 0

Tricarboxylic Acid (TCA) Cycle Enzyme Alpha-Ketoglutarate Dehydrogenase (KGDH) as a Nexus for the Regulation of Macrophage Polarization 三羧酸（TCA）循环酶-酮戊二酸脱氢酶（KGDH）在巨噬细胞极化调节中的作用

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-07-05 DOI: 10.1002/jcb.70104

Meijing Li, Ryan J. Mailloux

{"title":"Tricarboxylic Acid (TCA) Cycle Enzyme Alpha-Ketoglutarate Dehydrogenase (KGDH) as a Nexus for the Regulation of Macrophage Polarization","authors":"Meijing Li, Ryan J. Mailloux","doi":"10.1002/jcb.70104","DOIUrl":"https://doi.org/10.1002/jcb.70104","url":null,"abstract":"<p>Macrophage metabolism has been increasingly studied in recent years for its potential as a therapeutic target across multiple pathologies. In this article, we propose that the tricarboxylic acid (TCA) cycle enzyme alpha-ketoglutarate (KG) dehydrogenase (KGDH) serves as a nexus for regulating macrophage polarization toward pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes. This is achieved through modulation of mitochondrial hydrogen peroxide (mtH<sub>2</sub>O<sub>2</sub>) and the availability of the TCA cycle metabolites KG and succinate, which are important immunomodulatory molecules. We discuss the evidence showing KGDH is a potent source of mtH<sub>2</sub>O<sub>2</sub> in various cell types and how it could use this reactive oxygen species (ROS) to modulate signaling pathways involved in macrophage differentiation. Coupled to this, we describe emerging evidence showing that KG and succinate exert opposite signaling effects in macrophages, with the former metabolite inducing an anti-inflammatory phenotype and the latter (succinate) promoting inflammation. This occurs through the regulation of dioxygenases involved in hypoxic signaling and epigenetic programming and the activation of G-protein coupled receptor 91 (GPR91) by succinate. Importantly, we contend that regulating KGDH influences the availability of these two metabolites, which, along with controlling mtH<sub>2</sub>O<sub>2</sub> availability, helps control macrophage polarization. Collectively, increased mtH<sub>2</sub>O<sub>2</sub> generation and succinate are known to induce a pro-inflammatory phenotype, whereas low mtH<sub>2</sub>O<sub>2</sub> and high KG have the opposite effect. This suggests that KGDH is a key regulator of macrophage polarization by controlling the availabilities of these immunomodulatory metabolites.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"127 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70104","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148389192","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}

引用次数: 0

Zinc Finger Proteins as Regulators of Organ Fibrosis 锌指蛋白在器官纤维化中的调节作用。

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-06-23 DOI: 10.1002/jcb.70103

Bootsakorn Boonkaew, Wirawit Srivongtrakul, Chaiyaboot Ariyachet

{"title":"Zinc Finger Proteins as Regulators of Organ Fibrosis","authors":"Bootsakorn Boonkaew, Wirawit Srivongtrakul, Chaiyaboot Ariyachet","doi":"10.1002/jcb.70103","DOIUrl":"10.1002/jcb.70103","url":null,"abstract":"<div>\u0000 \u0000 <p>Organ fibrosis represents a terminal pathological consequence of chronic tissue injury and contributes substantially to global morbidity and mortality, yet effective therapeutic options remain limited. Characterized by the persistent activation of fibroblasts into myofibroblasts, fibrosis results in excessive extracellular matrix (ECM) deposition and progressive disruption of normal organ architecture, ultimately leading to functional failure. Increasing evidence places zinc finger proteins (ZNFs) as key mediators within the regulatory hierarchy of fibrotic diseases. As the largest and most diverse family of transcriptional regulators in the human genome, ZNFs utilize specialized zinc-coordinating motifs to regulate gene expression, protein stability, and intracellular signaling pathways. Beyond their classical roles in DNA binding and transcriptional control, ZNFs are now recognized as key orchestrators of fibrotic programs through regulation of ubiquitin-mediated protein turnover, cytoskeletal dynamics, and core pro-fibrotic signaling pathways, including transforming growth factor-β/Smad, mitogen-activated protein kinase, and phosphoinositide 3-kinase/protein kinase B cascades. Dysregulation of specific ZNFs has emerged as a critical driver of myofibroblast differentiation, ECM synthesis, and pathological tissue remodeling across multiple organ systems, including the liver, lung, kidney, skin, and heart. This review provides a comprehensive synthesis of the molecular roles of ZNFs in organ-specific fibrosis, integrating their structural classification with their mechanistic influence on key signaling networks. Furthermore, we discuss the clinical potential of ZNFs as biomarkers of fibrotic progression and evaluate emerging therapeutic strategies aimed at targeting ZNF-mediated pathways. Finally, we outline key knowledge gaps and future research directions. By consolidating recent advances, this review highlights ZNFs as promising molecular targets for the next generation of anti-fibrotic interventions.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"127 6","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148308310","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}

引用次数: 0