Cellular and Molecular Basis in Chronic Kidney Disease—2nd Edition

A Special Issue of Cells (ISSN 2073-4409) belonging to the section "Cellular Pathology".

Deadline for manuscript submissions: 30 October 2026 | Viewed by 935

Editors


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Guest Editor
Department of Medicine, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH 43614, USA
Interests: cardiovascular disease; atherosclerosis; endothelial dysfunction; chronic kidney disease; lipid metabolism; blood lipids
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Guest Editor
Department of Medical Microbiology and Immunology, University of Toledo, Toledo, OH, USA
Interests: medical microbiology and immunology; transplantation

Special Issue Information

Dear Colleagues,

Chronic kidney disease (CKD) remains a major global health burden and is characterized by the progressive loss of kidney function over time. Following the successful completion of our first Special Issue, we are pleased to launch a second edition to continue promoting scholarly exchange and advancing research in the field of CKD.

This new edition will further explore key mechanisms involved in CKD pathogenesis, including the renin–angiotensin–aldosterone system (RAAS), renal inflammation, fibrosis, and signaling pathways such as transforming growth factor beta 1 (TGF-β1), among others.

This Special Issue aims to provide a platform for the publication of original research articles and comprehensive reviews that enhance our understanding of the cellular and molecular mechanisms underlying CKD development and progression. We particularly welcome submissions addressing mechanistic insights, experimental models, biomarker discovery, translational research, and novel therapeutic strategies aimed at preventing or slowing CKD progression.

By bringing together innovative research findings and expert perspectives, this second edition seeks to foster collaboration and stimulate further advances in CKD research. We look forward to receiving your valuable contributions to this Special Issue.

Dr. Prabhatchandra Dube
Dr. Dulat Bekbolsynov
Guest Editors

Manuscript Submission Information

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Keywords

  • CKD
  • renal inflammation
  • renal fibrosis
  • RAAS
  • aldosterone
  • TGF-B1
  • uremic toxins
  • hypertension
  • GFR
  • albuminuria

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Published Papers (1 paper)

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Research

17 pages, 25378 KB  
Article
BPIFA2 Promotes Renal Fibrosis by Regulating Tubular Epithelial-to-Mesenchymal Transition and Macrophage Activation in Chronic Kidney Disease
by Xinyan Miao, Zecheng Lu, Xiaoqi Xing, Yuexin Tian, Jinxi Liu, Wei Zhang, Qingjuan Liu, Xiaojuan Feng and Shuxia Liu
Cells 2026, 15(12), 1093; https://doi.org/10.3390/cells15121093 - 16 Jun 2026
Viewed by 591
Abstract
Tubulointerstitial fibrosis (TIF) represents the final common pathway leading to end-stage renal disease (ESRD) in chronic kidney disease (CKD). Despite fibrosis being well established as a key pathological hallmark, the molecular mediators that drive this process remain incompletely understood. BPI fold-containing family A [...] Read more.
Tubulointerstitial fibrosis (TIF) represents the final common pathway leading to end-stage renal disease (ESRD) in chronic kidney disease (CKD). Despite fibrosis being well established as a key pathological hallmark, the molecular mediators that drive this process remain incompletely understood. BPI fold-containing family A member 2 (BPIFA2), a secreted innate immune protein of the sPLUNC family, was upregulated in renal tubular epithelial cells across diverse CKD etiologies and strongly correlated with collagen I accumulation and TIF severity. Tubule-specific knockdown of BPIFA2 significantly alleviated renal histopathological injury and fibrosis, whereas exogenous BPIFA2 administration aggravated fibrotic progression. Mechanistically, BPIFA2 promoted epithelial–mesenchymal transition (EMT) in tubular epithelial cells and triggered macrophage-to-myofibroblast transition (MMT) associated with the TGF-β/Smad3 signaling pathway. In conclusion, our findings identify BPIFA2 as a novel profibrotic mediator in CKD. Targeting BPIFA2 or its downstream signaling may offer new therapeutic opportunities for chronic kidney disease. Full article
(This article belongs to the Special Issue Cellular and Molecular Basis in Chronic Kidney Disease—2nd Edition)
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