Journal of Cellular Physiology最新文献_第5页

Corrigendum to “The Effects and Mechanisms of Myeloid Differentiation Protein 2 on Intestinal Mucosal Permeability in Mice With Chronic Colitis” 髓系分化蛋白 2 对慢性结肠炎小鼠肠黏膜通透性的影响和机制 "的更正

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-02-26 DOI: 10.1002/jcp.70009

{"title":"Corrigendum to “The Effects and Mechanisms of Myeloid Differentiation Protein 2 on Intestinal Mucosal Permeability in Mice With Chronic Colitis”","authors":"","doi":"10.1002/jcp.70009","DOIUrl":"https://doi.org/10.1002/jcp.70009","url":null,"abstract":"<p>Han C., Q. Guan, L. Guo, Y. Yang, S. Ruan, and X. Zhang. 2019. “The Effects and Mechanisms of Myeloid Differentiation Protein 2 on Intestinal Mucosal Permeability in Mice With Chronic Colitis.” <i>Journal of Cellular Physiology</i> 234, no. 11: 21089–21099. https://doi.org/10.1002/jcp.28711.</p><p>In the initial version of the proof stage, We mistakenly inserted incorrect panels in Figure 2d, Figure 3a, Figure 4d, Figure 5a, and Figure 6c. Specifically:</p><p>Figure 2c: We have confused the panels of Con and DSS, and the magnification is not consistent. We will present the correct results as follows:</p><p>Figure 3a: Strip insertion error for MD2. We will present the correct results as follows:</p><p>Figure 4d: TLR4 strip insertion error. We will present the correct results as follows:</p><p>Figure 5a: MD2 and GAPDH strip insertion error. We will present the correct results as follows:</p><p>Figure 6c: GAPDH strip insertion error. We will present the correct results as follows:</p><p>This correction doesn't change the results and conclusions. The authors apologize for any confusion these errors may have caused.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143490024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Comparative Single-Cell Analysis Reveals Tendon Progenitor Dysfunction by Age-Associated Oxidative Stress and Its Restoration by Antioxidant Treatments 比较单细胞分析揭示年龄相关氧化应激引起的肌腱祖细胞功能障碍及其通过抗氧化处理恢复

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-02-23 DOI: 10.1002/jcp.70016

Youngjae Jeong, Dongwook Yang, Jea Giezl Solidum, Laura Ortinau, Dongsu Park

{"title":"Comparative Single-Cell Analysis Reveals Tendon Progenitor Dysfunction by Age-Associated Oxidative Stress and Its Restoration by Antioxidant Treatments","authors":"Youngjae Jeong, Dongwook Yang, Jea Giezl Solidum, Laura Ortinau, Dongsu Park","doi":"10.1002/jcp.70016","DOIUrl":"https://doi.org/10.1002/jcp.70016","url":null,"abstract":"<div>\u0000 \u0000 <p>Impaired healing of adult tendons with fibrosis remains clinical challenges while neonatal tendons have full functional restoration. However, age-associated cellular and molecular changes in tendon cells and tendon stem/progenitor cells (TSPCs) remain unknown. Here, comparative single cell transcriptomics of early postnatal (2 weeks old) and adult (20 weeks old) mouse tendons revealed that adult tendons have reduced number of TSPCs, decreased gene expression in tendon and cartilage development, and a greater population of fibro-tenogenic cells. Notably, adult TSPCs and tenocytes exhibit increased expression of immune-response and oxidative-stress genes with higher EGFR but decreased IGF signaling. Adult tendon cells show increased levels of intracellular reactive oxygen species (ROS) in vivo. In contrast, antioxidant treatment of adult tendons significantly reduces intracellular ROS of TSPCs and improves tendon strength in vivo. Hence, these findings suggest that increased inflammation and ROS during tendon aging deteriorates tendon function and regeneration that can be mitigated by antioxidant treatment.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143475445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Trophic Factors in Muscle-Nerve Cross-Talk Signaling Augment Muscle Fiber and Motor Endplate Development 肌神经串扰信号中的营养因子促进肌纤维和运动终板的发育

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-02-23 DOI: 10.1002/jcp.70013

James T. Redden, Sophie Kothe, David J. Cohen, Zvi Schwartz, Michael J. McClure

{"title":"Trophic Factors in Muscle-Nerve Cross-Talk Signaling Augment Muscle Fiber and Motor Endplate Development","authors":"James T. Redden, Sophie Kothe, David J. Cohen, Zvi Schwartz, Michael J. McClure","doi":"10.1002/jcp.70013","DOIUrl":"https://doi.org/10.1002/jcp.70013","url":null,"abstract":"<div>\u0000 \u0000 <p>Synaptogenesis requires complex coordination between the terminating motor neuron and the developing myofiber endplate. Cross-talk research has focused on in vivo models or singular treatments with known signaling molecules identified from these animal studies. However, in vivo models are inefficient at measuring dynamic signaling changes due to assay resolution and cost. Further, despite advances in culture methods relying on microfluidic platforms, much remains unknown about the dynamic cross-talk between these two key cell types. As such, there is an unmet investigation into simple and reproducible coculture studies. In this study, we characterize both myoblast (C2C12) and motor neuron (NSC-34) changes that occur in either a conditioned media model, a transwell coculture, and a 2D migration coculture. We successfully demonstrate repeatable changes in synaptogenesis with ~38% increase in Chrng protein levels (<i>p</i> < 0.05) in each model, increased myotube alignment in cocultured myoblasts measured with FFT analysis, and show motor neurons are preferentially chemo-attracted to myotubes without the use of neurite-path constraining microfluidics. Lastly, we identified a potential new signaling protein responsible for motor endplate development, apolipoprotein E (ApoE). This coculture approach reveals changes to myotube myogenesis and synaptogenesis providing a consistent platform for cross-talk and pathway analysis for future studies.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143475444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Role of Metabolic Sensor GPR81/HCAR1 in Diabetic Podocytes: Downregulated Lipolysis Results in the Deterioration of Glomerular Filtration Barrier 代谢传感器GPR81/HCAR1在糖尿病足细胞中的作用：下调脂肪分解导致肾小球滤过屏障恶化

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-02-17 DOI: 10.1002/jcp.70014

Klaudia Grochowalska, Maria Szrejder, Patrycja Rachubik, Irena Audzeyenka, Dorota Rogacka, Magdalena Narajczyk, Agnieszka Piwkowska

{"title":"Role of Metabolic Sensor GPR81/HCAR1 in Diabetic Podocytes: Downregulated Lipolysis Results in the Deterioration of Glomerular Filtration Barrier","authors":"Klaudia Grochowalska, Maria Szrejder, Patrycja Rachubik, Irena Audzeyenka, Dorota Rogacka, Magdalena Narajczyk, Agnieszka Piwkowska","doi":"10.1002/jcp.70014","DOIUrl":"https://doi.org/10.1002/jcp.70014","url":null,"abstract":"<div>\u0000 \u0000 <p>The effacement of podocyte foot processes, which form slit diaphragms, are common features of proteinuria. Exploring podocyte energy metabolism, especially under diabetic conditions, may offer insights into the pathogenesis of diabetic kidney disease. Lipid accumulation is recognized as a cause of podocyte cytoskeleton remodeling and insulin resistance. Thus, the role of the metabolic sensor G-protein-coupled receptor 81 (GPR81) was examined in the molecular pathway of lipid accumulation in podocytes under hyperglycemic conditions. It was discovered that hyperglycemia downregulated the cyclic adenosine monophosphate/protein kinase A signaling pathway, which downregulated the expression of adipose triglyceride lipase (ATGL). Perilipin 1 was also downregulated; simultaneously, lipid droplet accumulation was enhanced. Glycerol and free fatty acid concentrations were also reduced, providing evidence of lipolysis inhibition. Interestingly, the expression of GPR81 decreased under hyperglycemia conditions despite the evidence of its activation, indicating strict lipolysis regulation. More importantly, cell functions were altered, reflected by an increase in albumin permeability and rearrangement of the actin cytoskeleton. The effect of ATGL activity inhibition on lipolysis, actin cytoskeleton arrangement, and permeability of the podocyte monolayer was investigated. The results were similar to GPR81 downregulation. Altogether, the present data indicate that GPR81 is likely a crucial part of the lipid sensing system, and its alterations during hyperglycemia might contribute to glomerular filtration barrier deterioration in diabetic kidney disease.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143431712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Single-Cell Transcriptome Decoding Umbilical Cord-Derived Mesenchymal Stem Cell Heterogeneity Reveals a Unique IL1R1HighPDGFRAHigh Ultroser-G-MSC With Osteogenesis and Chondrogenesis Signatures 单细胞转录组解码脐带来源的间充质干细胞异质性揭示了具有成骨和软骨形成特征的独特IL1R1HighPDGFRAHigh ultra - g - msc

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-02-16 DOI: 10.1002/jcp.70004

Shihao Huang, Xinyu Xu, Jiaqi Guo, Zhuolan Li, Yanlin Wu, Yuanyuan Liu, Qinyi Sun, Sihan Wang, Huilin Yan, Yueyan Su, Wei Guo

{"title":"Single-Cell Transcriptome Decoding Umbilical Cord-Derived Mesenchymal Stem Cell Heterogeneity Reveals a Unique IL1R1HighPDGFRAHigh Ultroser-G-MSC With Osteogenesis and Chondrogenesis Signatures","authors":"Shihao Huang, Xinyu Xu, Jiaqi Guo, Zhuolan Li, Yanlin Wu, Yuanyuan Liu, Qinyi Sun, Sihan Wang, Huilin Yan, Yueyan Su, Wei Guo","doi":"10.1002/jcp.70004","DOIUrl":"https://doi.org/10.1002/jcp.70004","url":null,"abstract":"<div>\u0000 \u0000 <p>The heterogeneity of human umbilical cord mesenchymal stem cells (hUC-MSCs) is culturing-dependent, resulting in functional non-uniformness. To achieve the best clinical benefit, a comprehensive understanding of the origin of the heterogeneity in different culture systems can identify functional subgroups to direct the precise application of hUC-MSCs. Here, we create a single-cell transcriptome atlas of hUC-MSC in different culture systems for the identification of a subgroup of Ultroser-G-MSCs with high osteogenic and chondrogenic potentials featured by high expressions of IL1R1 and PDGFRA. Further experimental validations surprisingly reveal that IL1R1<sup>high</sup>PDGFRA<sup>high</sup> Ultroser-G-MSCs possess advantages over “traditional” hUC-MSCs in the treatments of modeled osteoarthritis, leading to a cell-cell communication network centered in Clusters 0 and 2. Moreover, we found that Wnt5 signaling is the key pathway for the dynamic transformation of osteogenic and chondrogenic phenotypes in hUC-MSC. Overall, the present study paves the way for the clarification of heterogenetic nature of hUC-MSC in different culture systems for the selection of optimal MSC types to achieve the precision on clinical treatments.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143423727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Stearoyl-CoA Desaturase 1 Regulates Metabolism and Inflammation in Mouse Perivascular Adipose Tissue in Response to a High-Fat Diet 硬脂酰辅酶a去饱和酶1调节小鼠血管周围脂肪组织对高脂肪饮食的代谢和炎症反应

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-02-12 DOI: 10.1002/jcp.31510

Adrian Sowka, Volodymyr V. Balatskyi, Viktor O. Navrulin, James M. Ntambi, Pawel Dobrzyn

{"title":"Stearoyl-CoA Desaturase 1 Regulates Metabolism and Inflammation in Mouse Perivascular Adipose Tissue in Response to a High-Fat Diet","authors":"Adrian Sowka, Volodymyr V. Balatskyi, Viktor O. Navrulin, James M. Ntambi, Pawel Dobrzyn","doi":"10.1002/jcp.31510","DOIUrl":"https://doi.org/10.1002/jcp.31510","url":null,"abstract":"<div>\u0000 \u0000 <p>The dysregulation of perivascular adipose tissue (PVAT) is a key contributor to obesity-induced vascular dysfunction. Mouse periaortic adipose tissue is divided into two parts: thoracic perivascular adipose tissue (TPVAT) and abdominal perivascular adipose tissue (APVAT). These two parts have different physiological properties, which translate into different effects on the vascular wall in the onset of metabolic syndrome. Stearoyl-CoA desaturase 1 (SCD1) is an enzyme that is involved in the synthesis of monounsaturated fatty acids and has been shown to play an important role in metabolic syndrome, including vascular homeostasis. Despite a considerable focus on the role of SCD1 in the development of vascular disorders, there is currently a lack of knowledge of the relationship between SCD1 and PVAT. The present study investigated effects of SCD1 deficiency on lipolysis, β-oxidation, mitochondrial dynamics, and inflammation in mouse TPVAT and APVAT under high-fat diet (HFD) feeding conditions. We found lower triglyceride levels in PVAT in SCD1<sup>−/−</sup> mice both in vitro and in vivo compared with wildtype perivascular adipocytes, attributable to activated lipolysis and β-oxidation. Moreover, PVAT in HFD-fed SCD1<sup>−/−</sup> mice was characterized by higher levels of oxidative phosphorylation complexes and mitochondrial respiratory potential and alterations of mitochondrial morphology compared with wildtype mice. Furthermore, TPVAT and APVAT in SCD1<sup>−/−</sup> mice showed signs of greater pro-inflammatory macrophage polarization and higher inflammatory markers that were induced by a HFD. This may be related to the accumulation free fatty acids and diacylglycerols, which are enriched in saturated fatty acids. These findings elucidate the role of SCD1 in maintaining vascular integrity.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143396793","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Correction to “Effects of Photoperiod on Morphology and Function in Testis and Epididymis of Cricetulus Barabensis” 对“光周期对巴拉巴环鼠睾丸和附睾形态和功能的影响”的修正

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-02-12 DOI: 10.1002/jcp.70010

引用次数: 0

Proarrhythmic Lipid Inflammatory Mediators: Mechanisms in Obesity Arrhythmias 促心律失常的脂质炎症介质：肥胖症心律失常的机制

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-02-12 DOI: 10.1002/jcp.70012

Pegah Bahrami, Kelly A. Aromolaran, Ademuyiwa S. Aromolaran

{"title":"Proarrhythmic Lipid Inflammatory Mediators: Mechanisms in Obesity Arrhythmias","authors":"Pegah Bahrami, Kelly A. Aromolaran, Ademuyiwa S. Aromolaran","doi":"10.1002/jcp.70012","DOIUrl":"https://doi.org/10.1002/jcp.70012","url":null,"abstract":"<p>The prevalence of obesity and associated metabolic disorders such as diabetes is rapidly increasing; therefore, concerns regarding their cardiovascular consequences, including cardiac arrhythmias, are rising. As obesity progresses, the excessively produced lipids accumulate in unconventional areas such as the epicardial adipose tissue (EAT) around the myocardium. Metabolic alterations in obesity contribute to the transformation of these ectopic fat deposits into arrhythmogenic substrates. However, despite advances in therapeutic approaches, particularly in lowering EAT volume and thickness through sodium-glucose co-transporter-2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP-1) receptor agonists, obese and diabetic patients still suffer from fatal arrhythmias that may lead to sudden cardiac death. Therefore, an investigation into how unappreciated underlying pathways such as lipid mediators contribute to the transformation of adipose tissues into proinflammatory and arrhythmogenic substrates is of significance. Leukotriene B4 (LTB4) is an eicosanoid derived from arachidonic acid and acts as a lipid mediator. LTB4 has recently been identified to be associated with cardiac ion channel modulations and arrhythmogenic conditions in diabetes. LTB4 increases circulatory free fatty acids (FFAs) and has been associated with adipocyte hypertrophy. LTB4 also interferes with insulin signaling pathways, instigating insulin resistance (IR). In addition, LTB4, as a potent chemoattractant, contributes to the mobilization of circulatory immune cells such as monocytes and promotes inflammatory macrophage polarization and macrophage dysfunction. Thus, this review provides a comprehensive overview of LTB4's underlying pathways in obesity; illustrates how these pathways might lead to alterations in cardiac ion channels, currents, and cardiac arrhythmias; and shows how they might pose a therapeutic target for metabolic-associated arrhythmias.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143396977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Molecular Mechanisms and Therapeutic Implications of Long Non-coding RNAs in Cutaneous Biology and Disease 长链非编码rna在皮肤生物学和疾病中的分子机制和治疗意义

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-02-12 DOI: 10.1002/jcp.70006

Alessandro Zuccotti, Farah Al-Fatyan, Giulia D. S. Ferretti, Irene Bertolini, David T. Long, Ozgur Sahin, Jezabel Rodriguez-Blanco, Thibaut Barnoud

{"title":"Molecular Mechanisms and Therapeutic Implications of Long Non-coding RNAs in Cutaneous Biology and Disease","authors":"Alessandro Zuccotti, Farah Al-Fatyan, Giulia D. S. Ferretti, Irene Bertolini, David T. Long, Ozgur Sahin, Jezabel Rodriguez-Blanco, Thibaut Barnoud","doi":"10.1002/jcp.70006","DOIUrl":"https://doi.org/10.1002/jcp.70006","url":null,"abstract":"<div>\u0000 \u0000 <p>Human skin is the largest organ of the human body and accounts for approximately fifteen percent of the total bodyweight. Its main physiological role is to protect the body against a wide range of environmental factors including pathogens, ultraviolet light, and injury. Importantly, the skin can regenerate and heal upon injury in large part by the differentiation of keratinocytes. Not surprisingly, dysregulation of cutaneous differentiation and self-renewal can result in a variety of skin-related pathologies, including autoimmune disease and cancer. Increasing evidence supports the premise that long non-coding RNAs (lncRNAs) act as critical mediators of gene expression and regulate important biological processes within the skin. Notably, dysregulation of lncRNAs has been shown to influence diverse physiological and pathological consequences. More recently, numerous reports have revealed new mechanistic insight on the role that lncRNAs play in skin homeostasis as well as their contribution to the pathogenesis of skin-related disorders. Here, we review the biological functions of cutaneous lncRNAs and their impact on skin homeostasis. We also describe the fundamental roles of lncRNAs in the pathogenesis of skin-related disorders, including fibrotic, autoimmune, and malignant diseases. Lastly, we will highlight how a better understanding of lncRNAs at the molecular level may reveal novel therapeutic approaches for the improvement of cutaneous disorders.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143396792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Unraveling pH Regulation of TMEM175, an Endolysosomal Cation Channel With a Role in Parkinson's Disease 揭示TMEM175的pH调节，一个内溶酶体阳离子通道在帕金森病中的作用

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-02-04 DOI: 10.1002/jcp.70008

Tobias Schulze, Oliver Rauh, Gerhard Thiel, Niels Fertig, Andre Bazzone, Christian Grimm

{"title":"Unraveling pH Regulation of TMEM175, an Endolysosomal Cation Channel With a Role in Parkinson's Disease","authors":"Tobias Schulze, Oliver Rauh, Gerhard Thiel, Niels Fertig, Andre Bazzone, Christian Grimm","doi":"10.1002/jcp.70008","DOIUrl":"https://doi.org/10.1002/jcp.70008","url":null,"abstract":"<p>Transmembrane protein 175 (TMEM175) is an endolysosomal cation channel, which has attracted much attention recently from academics and the pharmaceutical industry alike since human mutations in TMEM175 were found to be associated with the development of Parkinson's disease (PD). Thus, gain-of-function mutations were identified, which reduce and loss-of-function mutations, which increase the risk of developing PD. After having been characterized as an endolysosomal potassium channel initially, soon after TMEM175 was claimed to act as a proton channel. In fact, recent evidence suggests that depending on the conditions, TMEM175 can act as either a potassium or proton channel, without acting as an antiporter or exchanger. A recent work has now identified amino acid H57 to be directly involved in gating, increasing proton conductance of the channel while leaving the potassium conductance unaffected. We review here the current knowledge of TMEM175 function, pharmacology, physiology, and pathophysiology. We discuss the potential of this ion channel as a novel drug target for the treatment of neurodegenerative diseases such as PD, and we discuss the discovery of H57 as proton sensor.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143111716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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