Mechanisms and Novel Therapeutic Approaches for Nephrology

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 August 2026 | Viewed by 4410

Editor


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Guest Editor
Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
Interests: podocyte injury; chronic kidney disease; acute kidney injury; proteinuria; hypertensive nephropathy

Special Issue Information

Dear Colleagues,

Chronic kidney disease (CKD) and acute kidney injury (AKI) represent significant global health burdens, with rising prevalence and limited therapeutic options. Advances in understanding the molecular mechanisms underlying kidney diseases, along with the development of innovative therapies, are critical to improving patient outcomes. This Special Issue seeks to highlight cutting-edge research in nephrology, focusing on mechanistic insights and emerging treatments that could transform clinical practice.

The aim of this Special Issue is to compile high-quality research and reviews on the pathophysiology of kidney diseases and novel therapeutic strategies, including pharmacological, cellular, and technological innovations. This topic aligns with the journal’s scope of publishing impactful translational and clinical research in nephrology. We encourage submissions that explore molecular pathways, biomarkers, drug discovery, and regenerative approaches to address unmet needs in kidney care.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following:

  • Molecular mechanisms of kidney injury and repair.
  • Novel biomarkers for early diagnosis and prognosis.
  • Pharmacological and biotechnological therapies for CKD and AKI.
  • Advances in dialysis and kidney transplantation.
  • Stem cell and regenerative medicine applications in nephrology.
  • Precision medicine and personalized treatment approaches.

We look forward to receiving your contributions.

Dr. Fang-Fang He
Guest Editor

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Keywords

  • chronic kidney disease
  • acute kidney injury
  • therapeutics
  • molecular mechanisms
  • biomarkers
  • drug discovery
  • regenerative medicine
  • precision medicine

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Published Papers (2 papers)

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Review

20 pages, 1658 KB  
Review
Rho/ROCK Signaling Pathway in Kidney Diseases: Mechanisms and Therapeutic Perspectives
by Wei Xiong, Daojia Miao, Zongchen Hou, Xiaoping Zhang and Zhiyong Xiong
Biomedicines 2026, 14(3), 621; https://doi.org/10.3390/biomedicines14030621 - 10 Mar 2026
Viewed by 1154
Abstract
Rho GTPases are a group of guanosine triphosphate (GTP)-binding proteins with a relative molecular weight of about 20–30 kD, and 22 different Rho GTPases have been identified in mammalian cells, among which RhoA, Rac1 and Cdc42 are the most well-studied. Rho-associated coiled coil [...] Read more.
Rho GTPases are a group of guanosine triphosphate (GTP)-binding proteins with a relative molecular weight of about 20–30 kD, and 22 different Rho GTPases have been identified in mammalian cells, among which RhoA, Rac1 and Cdc42 are the most well-studied. Rho-associated coiled coil forming protein kinase (ROCK) is the most well-researched downstream effector of Rho GTPases. The Rho/ROCK signaling pathway widely participates in the reorganization of the cytoskeleton through cascade phosphorylation/dephosphorylation reactions and modulates cellular biological behaviors including cell adhesion, migration and phenotypic transformation. Abnormal activation of the Rho/ROCK signaling pathway is closely associated with the occurrence and progression of acute kidney injury, diabetic nephropathy, hypertension-related nephropathy and chronic allograft nephropathy, which contributes to podocyte injury, renal tubular epithelial-to-mesenchymal transition (EMT), mesangial cell proliferation and inflammatory infiltration in the kidney. This review focuses on the research progress and regulatory mechanisms of the Rho/ROCK signaling pathway in the above four major kidney diseases and discusses the therapeutic potential of targeting this pathway for kidney disease treatment, aiming to provide new insights for elucidating the pathogenesis of kidney diseases and developing novel therapeutic strategies. Full article
(This article belongs to the Special Issue Mechanisms and Novel Therapeutic Approaches for Nephrology)
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36 pages, 1778 KB  
Review
Hypertension-Induced Renal Injury: From Pathophysiology to Therapeutic Perspectives
by Ning Zhou, Su-Ye Zhong, Pan Gao, Fang-Fang He and Chun Zhang
Biomedicines 2026, 14(3), 595; https://doi.org/10.3390/biomedicines14030595 - 6 Mar 2026
Cited by 2 | Viewed by 2794
Abstract
Hypertension-induced renal injury is a major cause of chronic kidney disease and end-stage renal disease. Increasing evidence indicates that disease progression is not driven solely by hemodynamic stress but results from the interplay of multiple molecular mechanisms. In this review, we propose a [...] Read more.
Hypertension-induced renal injury is a major cause of chronic kidney disease and end-stage renal disease. Increasing evidence indicates that disease progression is not driven solely by hemodynamic stress but results from the interplay of multiple molecular mechanisms. In this review, we propose a stage-structured and network-based framework to systematically integrate current mechanistic insights into hypertension-induced renal injury. Early events, mainly including endothelial dysfunction and renal hypoxia, establish a permissive microenvironment for disease progression. These insults activate amplifying pathways such as the renin–angiotensin–aldosterone system (RAAS) overactivation, oxidative stress, immune and inflammatory responses, and sympathetic nervous system hyperactivity, which interact through cross-talk and positive feedback loops. Ultimately, these signals converge on fibrotic programs characterized by epithelial–mesenchymal transition (EMT), fibroblast activation, and extracellular matrix deposition, leading to irreversible structural remodeling and functional decline. Furthermore, epigenetics, the gut–kidney axis, autophagy dysfunction and renal aging also contribute to this process. We highlight two critical and underappreciated aspects: the existence of a permissive ‘early-window’ dominated by endothelial dysfunction and hypoxia, which sets the stage for later amplification; and the hierarchical interplay between amplifying mechanisms where cross talk creates self-reinforcing loops that may explain therapeutic resistance. In addition, this review highlights emerging biomarkers for early diagnosis and disease monitoring, and discusses therapeutic advances that extend beyond blood pressure control to disease-modifying interventions that confer renoprotective effects. By integrating molecular mechanisms with diagnostic and therapeutic perspectives, this review provides a comprehensive framework for early detection and precision intervention in hypertension-induced renal injury. Full article
(This article belongs to the Special Issue Mechanisms and Novel Therapeutic Approaches for Nephrology)
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