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Biology
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Physiology and Pathophysiology of the Kidney
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Physiology and Pathophysiology of the Kidney

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Physiology".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 2193

Special Issue Editor

Dr. Gang Liu

E-Mail Website
Guest Editor
Department of Pathology & Laboratory Medicine, Tulane University School of Medicine, New Orleans, LA 70112, USA
Interests: autophagy; extracellular vesicles; kidney; liver; pathology; pathogenesis

Special Issue Information

Dear Colleagues,

It is with great pleasure that I extend an invitation to you to contribute to our upcoming Special Issue, “Physiology and Pathophysiology of the Kidney”. As the Guest Editor for this edition, I am excited to bring together leading experts to explore and advance our understanding of the intricate mechanisms underlying kidney function and dysfunction.

The kidneys play a pivotal role in maintaining homeostasis within the body, regulating fluid and electrolyte balance, blood pressure, and overall metabolic stability. This Special Issue aims to delve into the latest advances and discoveries in renal physiology and pathophysiology, spanning a wide range of topics including but not limited to renal hemodynamics and filtration, tubular transport mechanisms, renal endocrinology, renal development and regeneration, and kidney diseases and disorders.

We welcome original research articles, reviews, and perspective pieces that contribute to the advancement of knowledge in the field. All submitted manuscripts will undergo a rigorous peer-review process to ensure the highest quality of published articles. Our esteemed panel of reviewers will provide constructive feedback to authors, fostering collaboration and knowledge exchange.

Thank you for considering this invitation, and I eagerly anticipate your insightful contributions.

Dr. Gang Liu
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • renal physiology
  • renal hemodynamics
  • kidney injury
  • regenerative therapies
  • urology

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

13 pages, 1203 KiB  
Article
Small Extracellular Vesicles with a High Sphingomyelin Content Isolated from Hypertensive Diabetic db/db Mice Inhibits Calcium Mobilization and Augments Amiloride-Sensitive Epithelial Sodium Channel Activity
by Hunter Ramsay, Ling Yu, Faisal F. Alousi and Abdel A. Alli
Biology 2025, 14(3), 252; https://doi.org/10.3390/biology14030252 - 1 Mar 2025
Cited by 1 | Viewed by 469
Abstract
Extracellular vesicles (EVs) contain bioactive lipids that play a key role in pathophysiology. We hypothesized that EVs released from salt-loaded hypertensive diabetic db/db mice have increased bioactive lipid content that inhibits intracellular calcium mobilization and increases the activity of renal epithelial sodium channels [...] Read more.
Extracellular vesicles (EVs) contain bioactive lipids that play a key role in pathophysiology. We hypothesized that EVs released from salt-loaded hypertensive diabetic db/db mice have increased bioactive lipid content that inhibits intracellular calcium mobilization and increases the activity of renal epithelial sodium channels (ENaC). An enrichment of sphingomyelins (SMs) was found in small urinary EVs (uEVs) isolated from salt-loaded hypertensive diabetic db/db mice (n = 4) compared to non-salt loaded db/db mice with diabetes alone (n = 4). Both groups of mice were included in the same cohort to control for variability. Cultured mouse cortical collecting duct (mpkCCD) cells loaded with a calcium reporter dye and challenged with small uEVs from hypertensive diabetic db/db mice showed a decrease in calcium mobilization when compared to cells treated with small uEVs from diabetic db/db mice. The amiloride-sensitive transepithelial current was increased in mpkCCD cells treated with small uEVs with abundant sphingomyelin content from hypertensive diabetic db/db mice in a dose- and time-dependent manner. Similar results were observed in mpkCCD cells and Xenopus 2F3 cells treated with exogenous sphingomyelin in a time-dependent manner. Single-channel patch clamp studies showed a decrease in ENaC activity in cells transiently transfected with sphingomyelin synthase 1/2 specific siRNA compared to non-targeting siRNA. These data suggest EVs with high sphingomyelin content positively regulate renal ENaC activity in a mechanism involving an inhibition of calcium mobilization. Full article
(This article belongs to the Special Issue Physiology and Pathophysiology of the Kidney)
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14 pages, 2610 KiB  
Article
Effect of Riociguat on Adenine-Induced Chronic Kidney Disease in Rats
by Aly M. Abdelrahman, Raya Al Maskari, Haytham Ali, Priyadarsini Manoj and Yousuf Al Suleimani
Biology 2025, 14(2), 161; https://doi.org/10.3390/biology14020161 - 6 Feb 2025
Viewed by 811
Abstract
Riociguat is a soluble guanylate cyclase (sGC) activator that increases the levels of cyclic guanosine monophosphate (cGMP). cGMP is known to play a key role in regulating kidney function. This research sought to investigate the possible protective effects of riociguat on the kidneys [...] Read more.
Riociguat is a soluble guanylate cyclase (sGC) activator that increases the levels of cyclic guanosine monophosphate (cGMP). cGMP is known to play a key role in regulating kidney function. This research sought to investigate the possible protective effects of riociguat on the kidneys in the context of chronic kidney disease (CKD). CKD was induced in male Wistar rats through adenine administration. A total of 24 rats were allocated into four groups and administered treatments over a period of 35 days. Group 1 received a normal diet and a vehicle (carboxymethylcellulose (0.5%)), serving as the control. Group 2 received adenine (0.25% w/w) in the feed and a vehicle. Groups 3 and 4 received adenine in the feed (0.25% w/w) plus riociguat (3 mg/kg/day) and riociguat (10 mg/kg/day), respectively. Adenine administration significantly elevated systolic blood pressure, plasma creatinine, urea, and neutrophil gelatinase-associated lipocalin (NGAL). Furthermore, adenine reduced creatinine clearance and increased the urinary albumin-to-creatinine ratio and urinary N-Acetyl-β-D-Glucosaminidase (NAG). Histopathologically, adenine caused renal tubular necrosis and fibrosis. Furthermore, adenine elevated the plasma concentration of interleukins (IL-1β and IL-6) and tumor necrosis factor-alpha (TNF-α). Adenine significantly increased renal malondialdehyde (MDA) and reduced glutathione reductase (GR), superoxide dismutase (SOD), catalase (CAT), and total antioxidant capacity (TAC). Treatment with riociguat attenuated adenine-induced hypertension, improved kidney function, and ameliorated histopathological changes. Riociguat also reduced kidney injury markers, inflammation, and renal oxidative stress. The renoprotective effect of riociguat is probably due to anti-inflammatory and antioxidant actions. This indicates that riociguat may have the potential to slow the progression of kidney damage in chronic kidney disease (CKD). Full article
(This article belongs to the Special Issue Physiology and Pathophysiology of the Kidney)
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