ReviewStem cells international2026
Renovascular Disease and Its Impact on Endogenous Kidney Repair: Stem/Progenitor Cells.
Review in Stem cells international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
3 authors.
Funding
Abstract
Background: Renovascular disease (RVD), a progressive condition characterized by narrowing or occlusion of the renal arteries, is an important cause of secondary hypertension and chronic kidney disease (CKD) in older adults, associated with high cardiovascular morbidity and mortality. Recent evidence suggests that RVD compromises renal repair by impairing complementary vascular, stromal, and tubular repair systems, including endothelial progenitor cells (EPCs), mesenchymal stem/stromal cells (MSCs), and tubular regenerative pathways. Summary: RVD exposes these endogenous repair cells to multiple injurious stressors, including renal ischemia, hypertension, mechanical stretch, renin-angiotensin-aldosterone system (RASS) activation, and hypoxia. These upstream stressors trigger convergent cellular mechanisms, including oxidative stress, mitochondrial dysfunction, epigenetic and post-transcriptional (mRNA/miRNA) alterations, endoplasmic reticulum (ER) stress, cellular senescence, and apoptosis, leading to impaired reparative capacity. Cardiovascular comorbidities, including obesity, diabetes, and metabolic syndrome (MetS), further exacerbate these maladaptive responses. Experimental studies suggest that mitoprotective agents, epigenetic and miRNA modulators, ER-stress inhibitors, and extracellular vesicle (EV)-based therapies may preserve or restore stem/progenitor cell function. Key Messages: This review summarizes the current understanding of the impact of RVD on endogenous renal repair, focusing on the complementary roles of EPCs, MSCs, and tubular regenerative pathways, including resident renal progenitor cells, scattered tubular-like cells (STCs), and injury-induced epithelial plasticity. We discuss how common pathological stressors converge on shared molecular pathways to impair endogenous repair and highlight emerging therapeutic strategies aimed at preserving or restoring the regenerative capacity of these endogenous repair systems.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.