{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T18:07:27Z","timestamp":1791223647808,"version":"4.1.0"},"reference-count":60,"publisher":"American Society for Clinical Investigation","issue":"13","license":[{"start":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T00:00:00Z","timestamp":1783468800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000024","name":"Canadian Institutes of Health Research","doi-asserted-by":"crossref","award":["PJT\u2010155985"],"award-info":[{"award-number":["PJT\u2010155985"]}],"id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100005242","name":"Universit\u00e9 de Montr\u00e9al","doi-asserted-by":"crossref","award":["Shire Chair in Nephrology"],"award-info":[{"award-number":["Shire Chair in Nephrology"]}],"id":[{"id":"10.13039\/501100005242","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100013367","name":"Fondation Jean-Louis L\u00e9vesque","doi-asserted-by":"crossref","award":["NA"],"award-info":[{"award-number":["NA"]}],"id":[{"id":"10.13039\/100013367","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,7,8]]},"abstract":"<jats:p>\n                    Ischemia-reperfusion injury (IRI) is a common cause of acute kidney injury (AKI) leading to renal fibrosis. Here, we investigate the kinetics of autophagy, apoptosis, and necroptosis activation in tubular epithelial cells (TECs) and peritubular capillaries (PTCs) after renal IRI, and their relative contributions to renal fibrogenesis. IRI with renal artery clamping in GFP-LC3 transgenic mice induced a predominant and sustained necroptotic response in TECs, while apoptosis and autophagy played minor roles. PTCs showed early and persistent activation of apoptosis, brief necroptosis induction, and increased autophagy at a distance from IRI. Disruption of the autophagic process with chloroquine (CHQ) injections in association with renal IRI did not modulate tubular death but enhanced PTC apoptosis and increased microvascular rarefaction and fibrosis. Apoptosis-deficient GFP-LC3\n                    <jats:italic>\n                      \/Caspase-3\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    <\/jats:italic>\n                    mice exposed to renal IRI showed enhanced PTC autophagy, reduced PTC rarefaction, and inhibition of renal fibrosis, in spite of increased necroptosis in TECs. Inhibition of both autophagy with CHQ and apoptosis in GFP-LC3\n                    <jats:italic>\n                      \/Caspase-3\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    <\/jats:italic>\n                    mice led to a marked switch toward necroptosis in PTCs. This was associated with aggravated microvascular rarefaction, increased leukocyte infiltration, and enhanced renal fibrosis. These findings establish a predominant role for PTC autophagy and caspase-3\u2013dependent apoptosis in the development of renal fibrosis after IRI.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.201945","type":"journal-article","created":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T18:01:02Z","timestamp":1783447262000},"source":"Crossref","is-referenced-by-count":1,"title":["Microvascular autophagy and caspase-3 activation are central regulators of renal fibrosis after ischemia-reperfusion"],"prefix":"10.1172","volume":"11","author":[{"given":"Hyunyun","family":"Kim","sequence":"first","affiliation":[{"name":"D\u00e9partement de M\u00e9decine, Universit\u00e9 de Montr\u00e9al, Montr\u00e9al, Quebec, Canada."},{"name":"Centre de Recherche, Centre Hospitalier de l\u2019Universit\u00e9 de Montr\u00e9al (CRCHUM), Montr\u00e9al, Quebec, Canada."},{"name":"Canadian Donation and Transplantation Research Program (CDTRP), University of Alberta, Edmonton, Alberta, 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