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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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Summary<\/jats:title>\n                    <jats:p>RVD exposes these endogenous repair cells to multiple injurious stressors, including renal ischemia, hypertension, mechanical stretch, renin\u2013angiotensin\u2013aldosterone system (RASS) activation, and hypoxia. These upstream stressors trigger convergent cellular mechanisms, including oxidative stress, mitochondrial dysfunction, epigenetic and post\u2010transcriptional (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\u2010stress inhibitors, and extracellular vesicle (EV)\u2010based therapies may preserve or restore stem\/progenitor cell function.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Messages<\/jats:title>\n                    <jats:p>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\u2010like cells (STCs), and injury\u2010induced 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.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1155\/sci\/4007512","type":"journal-article","created":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T11:04:41Z","timestamp":1790766281000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Renovascular Disease and Its Impact on Endogenous Kidney Repair: Stem\/Progenitor Cells"],"prefix":"10.1155","volume":"2026","author":[{"given":"Vinaya C.","family":"Iyer","sequence":"first","affiliation":[{"name":"Division of Nephrology and Hypertension Mayo Clinic  Rochester Minnesota USA  mayo.edu"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3271-3887","authenticated-orcid":false,"given":"Lilach O.","family":"Lerman","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension Mayo Clinic  Rochester Minnesota USA  mayo.edu"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3864-9644","authenticated-orcid":false,"given":"Alfonso","family":"Eirin","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension Mayo Clinic  Rochester Minnesota USA  mayo.edu"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,9,30]]},"reference":[{"key":"e_1_2_10_1_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM200102083440607"},{"key":"e_1_2_10_2_2","doi-asserted-by":"publisher","DOI":"10.1067\/mva.2002.127351"},{"key":"e_1_2_10_3_2","doi-asserted-by":"publisher","DOI":"10.1159\/000013340"},{"key":"e_1_2_10_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00406.x"},{"key":"e_1_2_10_5_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.0590041480.x"},{"key":"e_1_2_10_6_2","doi-asserted-by":"publisher","DOI":"10.1681\/ASN.V2111608"},{"key":"e_1_2_10_7_2","doi-asserted-by":"publisher","DOI":"10.1053\/j.ajkd.2016.12.004"},{"key":"e_1_2_10_8_2","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2001.24521"},{"key":"e_1_2_10_9_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2001.00953.x"},{"key":"e_1_2_10_10_2","doi-asserted-by":"publisher","DOI":"10.3109\/08037051.2010.527445"},{"key":"e_1_2_10_11_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2168.2002.02144.x"},{"key":"e_1_2_10_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ahj.2008.05.013"},{"key":"e_1_2_10_13_2","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/gfr496"},{"key":"e_1_2_10_14_2","doi-asserted-by":"publisher","DOI":"10.1159\/000107552"},{"key":"e_1_2_10_15_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa0905368"},{"key":"e_1_2_10_16_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1310753"},{"key":"e_1_2_10_17_2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.2012.363"},{"key":"e_1_2_10_18_2","doi-asserted-by":"publisher","DOI":"10.1097\/MNH.0b013e328363ffe0"},{"key":"e_1_2_10_19_2","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.123.21362"},{"key":"e_1_2_10_20_2","first-page":"51","article-title":"Induction of Heme Oxygenase-1 in Renovascular Hypertension Is Associated With Inhibition of Apoptosis","volume":"53","author":"Botros F. 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