Cellular Physiology and Biochemistry最新文献

{"title":"Identifying Circ-RNF216 as a Regulator of Renal Tubular Epithelial Cell Proliferation Via the TGF-Β1/Smad3-Mediated Pathway in Chronic Kidney Disease.","authors":"Minghui Xu, Yue Yang, Puhua Zhang, Chunxia Zhou, Qin Zhou, Ning Luo","doi":"10.33594/000000833","DOIUrl":"https://doi.org/10.33594/000000833","url":null,"abstract":"<p><strong>Background/aims: </strong>Emerging evidence suggests that circular RNAs (circRNAs) play a crucial role in kidney disease regulation. However, their functional significance in chronic kidney disease (CKD) remains poorly understood.</p><p><strong>Methods: </strong>In this study, circRNAs were identified by RNA sequencing in two CKD mouse models, including unilateral ureteral obstruction (UUO) and anti-glomerular basement membrane (anti-GBM) glomerulonephritis. RNase-R treatment and Sanger sequencing were used to confirm circular structure. Circ-RNF216-shRNA was used to establish stable knockdown mTEC cell lines. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect circ-RNF216 expression. In situ hybridization was used to assess the expression and localization of circ-RNF216 in kidney. Transwell assays were performed to assess cell migration. RNA sequencing was performed to characterize mRNA expression profiles and identify pathways affected by circ-RNF216 knockdown in mTECs.</p><p><strong>Results: </strong>We identified 1,589 circRNAs in two CKD mouse models. Circ-RNF216 expression was up-regulated in UUO models. Functional analyses revealed that circ-RNF216 regulates renal fibrosis through modulation of the TGF-β1/Smad3 pathway. Knocking down circ-RNF216 in mouse tubular epithelial cells led to significant suppression of migratory capacity and fibrosis. RNA sequencing showed that circ-RNF216 knockdown altered mRNA expression, with differentially expressed genes mainly enriched in the transforming growth factor-β receptor superfamily signaling pathway.</p><p><strong>Conclusion: </strong>Our findings highlight circ-RNF216 as a novel regulatory factor in CKD-related renal fibrosis, broadening our understanding of circRNA involvement in kidney disease pathogenesis and suggesting circ-RNF216 as a potential therapeutic target for preserving renal function.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"56 6","pages":"867-883"},"PeriodicalIF":2.0,"publicationDate":"2025-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145667192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Succinylation of CTBP1 Mediated by SIRT5 Suppresses MAT1A Expression to Promote the Progression of HCC.","authors":"Zhengcai Qiu, Qipeng Wang, Shangshang Li, Guang Lu, Jing Han","doi":"10.33594/000000832","DOIUrl":"https://doi.org/10.33594/000000832","url":null,"abstract":"<p><strong>Background/aims: </strong>Succinylation, a recently characterized post-translational modification (PTM), is a ubiquitously occurring protein modification implicated in diverse biological processes via regulation of protein function and gene expression. CTBP1 encodes C-terminal binding proteins and generates multiple splice variants. However, the functional significance of CTBP1 succinylation in hepatocellular carcinoma (HCC) remains unexplored.</p><p><strong>Methods: </strong>Protein succinylation levels were quantified using immunoprecipitation coupled with Western blotting and mass spectrometry. Site-directed mutagenesis identified critical lysine residues targeted by succinylation. Functional impacts of CTBP1 succinylation on HCC cell behaviors were evaluated through CCK8-based cell viability, wound healing, transwell migration, and invasion assays. Molecular mechanisms were elucidated via qRT-PCR and Western blot analyses.</p><p><strong>Results: </strong>Succinylation levels of CTBP1 were significantly elevated in HCC tumor tissues and cell lines relative to non-tumorous controls. Mass spectrometry and mutagenesis pinpointed K46 and K280 as the primary succinylation sites on CTBP1, with SIRT5 identified as the desuccinylase. Functionally, CTBP1 succinylation enhanced HCC cell proliferation, migration, and invasive potential. Mechanistically, this modification promoted tumor progression by suppressing MAT1A expression-a key regulator of hepatic differentiation and tumorigenesis.</p><p><strong>Conclusion: </strong>Our study reveals that SIRT5-mediated CTBP1 succinylation drives HCC progression through MAT1A suppression, establishing a novel regulatory axis with therapeutic potential for HCC treatment.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 6","pages":"857-866"},"PeriodicalIF":2.0,"publicationDate":"2025-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145667135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"3-Acetyl-11-Keto-Beta-Boswellic Acid Inhibits Adipogenesis by Suppressing Autophagy and Inducing AMPK Phosphorylation in 3T3-L1 Cells.","authors":"Faizullah Khan, Muhammad Waqas, Hassan Moghtaderi, Najeeb Ur Rehman, Satya Kumar Avula, Haroon Khan, Mahua Choudhury, Ahmed Al-Harrasi, Shaikh Mizanoor Rahman","doi":"10.33594/000000830","DOIUrl":"https://doi.org/10.33594/000000830","url":null,"abstract":"<p><strong>Background/aims: </strong>Adipogenesis involves preadipocyte differentiation and lipid droplet accumulation and is closely linked to obesity. 3-Acetyl-11-keto-beta-boswellic acid (AKBA), a frankincense-derived triterpene, has anti-inflammatory and anticancer properties, but its role in adipocyte differentiation remains unclear.</p><p><strong>Methods: </strong>3T3-L1 preadipocytes were induced to differentiate with or without varying concentrations of AKBA. Cell viability was assessed by MTT assay, lipid accumulation by Oil Red O staining, and apoptosis by annexin V-FITC assay. Expression of adipogenic transcription factors, lipid-associated proteins, apoptotic markers, autophagy-related proteins, and AMPK phosphorylation was analysed by Western blotting. Molecular docking was used to evaluate AKBA interactions with target proteins.</p><p><strong>Results: </strong>AKBA inhibited adipocyte differentiation by suppressing C/EBPβ, C/EBPα, and PPARγ expression, reduced lipid accumulation, increased apoptosis via an elevated Bax/Bcl2 ratio, suppressed autophagy markers ATG5 and LC3b, and enhanced AMPK phosphorylation. Docking studies suggested AKBA binding to PPARγ and ATG5.</p><p><strong>Conclusion: </strong>AKBA suppresses adipogenesis by inhibiting adipogenic transcription factors, autophagy, and activating AMPK, supporting its potential as an anti-obesity therapeutic candidate.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 6","pages":"826-840"},"PeriodicalIF":2.0,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145888197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary Vitamin E Ameliorate Production Performance Via Pyruvate Metabolism Regulation in An Aged Laying Quails.","authors":"Hongyan Chen, Mengqian Zou, Tingting Cui, Xiaotong Qin, Fei Gao, Shutong Deng, Zheng Chen, Qingying Li, Zhigang Wang","doi":"10.33594/000000829","DOIUrl":"https://doi.org/10.33594/000000829","url":null,"abstract":"<p><strong>Background/aims: </strong>This study aimed to clarify the optimal amount of vitamin E required in the late stage of egg laying to explore the aging mechanism of the ovaries in this stage and the regulatory role of vitamin E in female reproductive aging using multiple experimental methods and multiomics joint analysis.</p><p><strong>Methods: </strong>The development of follicles was analyzed using Hematoxylin-eosin staining and terminal deoxynucleotidyl transferase deoxyuridine phosphate nick-end labeling staining. The content of follicle-stimulating hormone (FSH), luteinizing hormone (LH) and Estradiol (E2) was determined by Enzyme-linked Immunoassay Kit. The activities of superoxide dismutase (SOD) and malondialdehyde (MDA) in the serum using enzyme-linked immunosorbent assay kits. RNA-seq and Untargeted metabolomics analyses were used to investigate the molecular mechanisms of vitamin E during ovarian aging.</p><p><strong>Results: </strong>The findings revealed that quail reproductive organs rapidly aged at the 11th egg-laying month. Adding vitamin E to the diet significantly improved egg production performance. Vitamin E promoted the development of small yellow follicles by enhancing antioxidant capacity and inhibiting cell apoptosis. Furthermore, RNA-seq and LC-MS/MS identified genes and metabolites that may serve as biomarkers for vitamin E effects.</p><p><strong>Conclusion: </strong>Dietary supplementation with 250 mg/kg vitamin E enhanced energy metabolism, regulated SOD and MDA levels, reduced apoptosis, stimulated E2 secretion, promoted follicular development, and improved egg production performance.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 6","pages":"811-825"},"PeriodicalIF":2.0,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145667109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor Destructive Mechanical Impulse (TMI) Treatment of Solid Tumors. Part I: Animal Experiments, Clinical Application and Immunological Abscopal Effect.","authors":"Axel Erich Theuer, Ioannis Thomas, Florian Lang, Maria Borkmann, John David Mullins, Thomas K Eigentler, Gerhard Franz Walter","doi":"10.33594/000000828","DOIUrl":"10.33594/000000828","url":null,"abstract":"<p><strong>Background/aims: </strong>The feasibility and effectiveness of Tumor Destructive Mechanical Impulse (TMI) treatment of solid tumors for standard clinical application is investigated.</p><p><strong>Methods: </strong>Different solid tumors in a preparatory animal experiment (VX2 head and neck squamous tumor) and in patients (malignant cutaneous melanoma and prostate carcinoma) are treated by TMI focused shock waves using patient-specific treatment parameters (total energy, energy flux density, shock wave frequency, total number and sequence of shock waves, the optimal placement of the treatment device) determined by multiple parametric simulations.</p><p><strong>Results: </strong>In animal experiments and in the different treated tumor entities in several patients, the treated tumor or treated metastases regressed, and disguised tumor-associated antigens consistently initiated an immunological abscopal effect achieving that not only the directly treated primary tumor or a treated metastasis regressed but also untreated distant metastases.</p><p><strong>Conclusion: </strong>TMI treatment could have significant implications for the development of new effective and targeted regimens of cancer therapy.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 6","pages":"800-810"},"PeriodicalIF":2.0,"publicationDate":"2025-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145494688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epistemology of the Origin of Cancer III: Fundamentals of How Metastasis Arises.","authors":"Björn L D M Brücher, Ijaz S Jamall","doi":"10.33594/000000826","DOIUrl":"https://doi.org/10.33594/000000826","url":null,"abstract":"<p><p>Metastasis, like carcinogenesis, involves the disruption of homeostasis such that cancer cells travel from the primary tumor to distant parts of the body. Almost all cancer deaths are due to metastatic spread. The prevailing theory of metastasis is an incomplete doctrine and far from sufficient as only 0.2% of free cancer cells result in the spread of cancer. To develop reasonable and effective cancer therapies and to prevent (or reverse) carcinogenesis and metastasis, a comprehensive understanding of how both carcinogenesis and metastasis arise is necessary. Fundamental questions in cancer biology have been asked and answered over decades of research: How do most cancers develop (Epistemology of the Origin of Cancer I, 2014-2022)? Which is the first cancer cell (II, 2023)? The third basic question in cancer biology remaining to be addressed is: What are the fundamentals of how metastasis develops? The pre-cancerous niche (PCN) that forms during carcinogenesis is altered by ongoing complex signaling into a premetastatic niche 1 (PMN-1): p130(cas)/crk/DOCK180 formation is necessary for lamellipodia formation, thereby enabling cell mobility. Cancer-associated fibroblasts (CAFs) begin to release fibronectin CXCL12 and Keratin 19. PMN-1 is transformed into PMN-2 during ongoing crosstalk and transformation of anti- into pro-tumorigenic platelets, macrophages, and neutrophils. Finally, persistent signaling and immune evasion result in the conversion of PMN-2 to PMN-3 with heterogeneous cancer satellites - the term \"satellite\" is used herein in accordance with its original meaning (a cell or particle escorting another). PMN-3 serves as a prerequisite for intravasation, traveling, and dissemination of cancer cells away from the primary tumor. Eight heterogeneous cancer satellites, including Trojan horses (immune evasion), travel alone or in combination: (1) cancer cells and (2) CAFs migrate along the CXCL12 and fibronectin gradient; (3) cancer cells surrounded by CAFs are shielded from the immune system and travel away from the primary cancer; (4) CXCL12 and Keratin 19 coat cancer cells; (5) platelets surround cancer cells and (6) CAFs, thereby facilitating cancer spread; and (7) neutrophil extracellular traps shield cancer cells and (8) CAFs. Metastasis in epithelial cancer occurs in parallel with carcinogenesis after the pre-cancerous niche is transformed into pre-metastatic niches (PMNs), which are indispensable to the origin of metastasis. Eight heterogeneous cancer satellites, including Trojan horses responsible for immune evasion, alongside reciprocally affecting sequences, wander alone or in conjunction with other cancer cells. This elucidates why the current practice of multimodal anti-cancer cell therapy should now be seen in a new light in which the benefits depend not on direct cancer cell effects, but on indirect cytopenic effects, which have previously been regarded merely as adverse effects.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 6","pages":"753-799"},"PeriodicalIF":2.0,"publicationDate":"2025-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145450989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of Novel Kv1.3 Channel-Interacting Proteins Using Proximity Labelling in T-Cells.","authors":"Dilpreet Kour, Christine A Bowen, Upasna Srivastava, Hai M Nguyen, Rashmi Kumari, Prateek Kumar, Amanda D Brandelli, Sara Bitarafan, Brendan R Tobin, Levi B Wood, Nicholas T Seyfried, Heike Wulff, Srikant Rangaraju","doi":"10.33594/000000823","DOIUrl":"10.33594/000000823","url":null,"abstract":"<p><strong>Background/aims: </strong>Potassium channels regulate membrane potential, calcium flux, cellular activation and effector functions of adaptive and innate immune cells. The voltage-activated Kv1.3 channel is an important regulator of T cell-mediated autoimmunity and microglia-mediated neuroinflammation. Kv1.3 channels, via protein-protein interactions, are localized with key immune proteins and pathways, enabling functional coupling between K+ efflux and immune mechanisms.</p><p><strong>Methods: </strong>To gain insights into proteins and pathways that interact with Kv1.3 channels, we applied a proximity-labeling proteomics approach to characterize protein interactors of the Kv1.3 channel in activated T-cells. Biotin ligase TurboID was fused to either N or C termini of Kv1.3, stably expressed in Jurkat T cells, and biotinylated proteins in proximity to Kv1.3 were enriched and quantified by mass spectrometry.</p><p><strong>Results: </strong>We identified over 1,800 Kv1.3 interactors including known interactors (beta-integrins, Stat1), although the majority were novel. We found that the N-terminus of Kv1.3 preferentially interacts with protein synthesis and protein trafficking machinery, while the C-terminus interacts with immune signaling and cell junction proteins. T-cell Kv1.3 interactors we found consisted of 335 cell surface proteins, including T-cell receptor complex, mitochondrial, calcium and cytokine-mediated signaling pathway, and lymphocyte migration proteins. 178 Kv1.3 interactors in T-cells also represent genetic risk factors for T cell-mediated autoimmunity, including STIM1, which was further validated using co-immunoprecipitation.</p><p><strong>Conclusion: </strong>Our studies revealed novel proteins and molecular pathways that interact with Kv1.3 channels in adaptive (T-cell) and innate (microglia) immune cells, providing a foundation for understanding how Kv1.3 channels may regulate immune mechanisms in autoimmune.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 S1","pages":"41-70"},"PeriodicalIF":2.5,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989817/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145586133","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":"B Cells at the Crossroads of Cardiovascular and Hematologic Disease: Paving the Way for Novel Immunomodulatory Therapies.","authors":"Angeliki Choustoulaki, Soumaya Ben-Aicha, Despina Fotiou, Alexandros Briasoulis, Ourania Tsitsilonis, Efstathios Kastritis, Panagiota Efstathia Nikolaou","doi":"10.33594/000000822","DOIUrl":"https://doi.org/10.33594/000000822","url":null,"abstract":"<p><p>The interaction between the immune and cardiovascular systems is a growing field of investigation with bidirectional aspects. B cells are modulators of the adaptive and the innate immunity and they orchestrate bone marrow and spleen immune responses beyond infectious diseases. B cell regulation contributes to the pathophysiology of myocardial damage in several conditions including myocardial infarction, heart failure and atherosclerosis. In parallel, B cell-derived hematological disorders are interlinked to cardiovascular complications, including thrombosis and immunoglobulin-related cardiotoxicity. The scope of this review is to summarize the function and role of B cells as important players in myocardial and vascular adaptations to injury and as mediators of cardiovascular adverse events in hematological disorders. The primary focus is to highlight the clinical and preclinical findings regarding B cell-targeted therapies and their positive or negative impact on the cardiovascular system. A deeper understanding of B cell subpopulations, functions, and secretome could lead to targeted therapeutic interventions for cardiovascular and hematologic diseases.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 S3","pages":"22-51"},"PeriodicalIF":2.0,"publicationDate":"2025-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145367660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Isobutylparaben and Phenylmercuric Acetate on Juvenile Female Rats with Special Reference to Development, Neurobehavior, and Histopathology.","authors":"Vishwajit B Darekar, Basawarajeshwari Indur","doi":"10.33594/000000821","DOIUrl":"https://doi.org/10.33594/000000821","url":null,"abstract":"<p><strong>Background/aims: </strong>Isobutylparaben (IBP) and phenylmercuric acetate (PMA) are extensively applied in pharmaceuticals, cosmetics, and industrial chemicals, and are of concern for developmental toxicity. This study was conducted to compare and assess the subchronic effects of IBP and PMA on growth, neurobehavior, reproduction, and organ integrity in juvenile female rats, and establish no-observed-adverse-effect levels (NOAELs).</p><p><strong>Methods: </strong>Juvenile female Sprague-Dawley rats (n=10/group) were given IBP (10, 20, 50 mg/kg/day) or PMA (2, 4, 8 mg/kg/day) by gavage for 70 days. Assays encompassed growth assessment, onset of puberty (vaginal opening), estrous cyclicity (vaginal smears), neurobehavioral examination (open-field activity, sensory reflexes, grip strength, motor activity), haematology, serum biochemistry, thyroid hormones (ELISA), organ weights, and histopathology of reproductive, hepatic, and renal tissues.</p><p><strong>Results: </strong>IBP and PMA at high doses significantly inhibited terminal body weight, postponed vaginal opening, disrupted motor function, and affected exploratory behavior. Biochemical indicators revealed hepatic and renal stress and histological findings of hepatocellular hypertrophy and renal tubular degeneration. PMA was somewhat more toxic. NOAELs were 20 mg/kg/day (IBP) and 4 mg/kg/day (PMA).</p><p><strong>Conclusion: </strong>Both IBP and PMA caused dose-dependent developmental toxicity, calling for more stringent pediatric exposure evaluations and chemical safety regulations.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 5","pages":"736-750"},"PeriodicalIF":2.0,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145888208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epithelial Impermeability to Water: A Second Look.","authors":"Lydia G Gibson, Elena K DeFilippo, Austin Mahajan, Michael A Model","doi":"10.33594/000000820","DOIUrl":"https://doi.org/10.33594/000000820","url":null,"abstract":"<p><p>Impermeability of the ascending limb of the Henle loop for water is traditionally regarded as essential for countercurrent multiplication in the kidney. Similar claims have been made about permeability properties of the collecting duct and some other epithelia. It is not clear, however, how a structure based on phospholipid bilayers can be water-impermeant if phospholipid bilayers themselves have measurable permeability. The presence of two membranes separated by the cytoplasm may only account for a several-fold reduction in permeability compared to a single bilayer. By analyzing published data, we conclude that these tubules do have a finite water permeability, especially the collecting duct. Although the results on isolated ascending limbs vary among authors, osmotic shock experiments clearly indicate that both the collecting duct and the ascending Henle loop are sufficiently water-permeable to observe volume regulation effects. We conclude that these epithelia by themselves do not display unusual resistance to water flow; it can be estimated that 20-50% of the fluid entering the tubules can be reabsorbed into a strongly hypertonic medulla. It is possible, however, that unstirred layers in the intact kidney may contribute to the apparent low permeability of the tubules.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 5","pages":"730-735"},"PeriodicalIF":2.0,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145367634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}