{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T07:20:17Z","timestamp":1790061617408,"version":"4.0.1"},"reference-count":47,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","funder":[{"DOI":"10.13039\/100000057","name":"National Institute of General Medical Sciences","doi-asserted-by":"crossref","award":["R35GM137984"],"award-info":[{"award-number":["R35GM137984"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"crossref","award":["T32DK007257"],"award-info":[{"award-number":["T32DK007257"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"crossref","award":["R56DK134582"],"award-info":[{"award-number":["R56DK134582"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"crossref","award":["R01DK135555"],"award-info":[{"award-number":["R01DK135555"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"crossref","award":["P30DK079328"],"award-info":[{"award-number":["P30DK079328"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000052","name":"NIH Office of the Director","doi-asserted-by":"crossref","award":["1S10OD021685-01A1"],"award-info":[{"award-number":["1S10OD021685-01A1"]}],"id":[{"id":"10.13039\/100000052","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100004917","name":"Cancer Prevention and Research Institute of Texas","doi-asserted-by":"crossref","award":["RP240494"],"award-info":[{"award-number":["RP240494"]}],"id":[{"id":"10.13039\/100004917","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["JASN"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:sec>\n                    <jats:title>Key Points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Proximal tubular expression of hydroxymethylglutaryl-CoA synthase 2 (HMGCS2) during ischemic injury increases kidney ketone and prostaglandin content.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Kidney HMGCS2 deficiency emerged as both a biomarker and contributor to kidney disease.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Renal ketogenesis supported the maintenance of proximal tubular fatty acid oxidation.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Abnormal renal fatty acid oxidation in kidney disease suggests that dysregulated metabolism is a key component of kidney disease pathogenesis. While the liver is the main ketogenic organ, the rate-limiting enzyme for ketogenesis, mitochondrial hydroxymethylglutaryl-CoA synthase 2 (HMGCS2), is induced in the proximal tubule of the kidney during fasting. We previously demonstrated that HMGCS2 induced in the kidney does not contribute to the circulating pool of ketones during fasting and cannot compensate for hepatic ketogenic deficiency. We hypothesized that kidney HMGCS2 may be acting locally within the kidney to maintain normal function during metabolic stress or injury.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Mice with kidney- or liver-specific deletion of\n                      <jats:italic toggle=\"yes\">Hmgcs2<\/jats:italic>\n                      were subjected to ischemia\/reperfusion injury (IRI). Kidney histology, metabolomics, and lipidomics were analyzed. Mice were placed on a ketogenic diet for 4 days to increase plasma and kidney ketone content. Using novel mouse models with proximal tubular hemagglutinin-tagged mitochondria with or without\n                      <jats:italic toggle=\"yes\">Hmgcs2<\/jats:italic>\n                      deletion, proximal tubular\u2013specific mitochondria were isolated, and fatty acid oxidation capacity was measured after IRI.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Mice with kidney-specific\n                      <jats:italic toggle=\"yes\">Hmgcs2<\/jats:italic>\n                      deletion had significantly more kidney injury after IRI compared with wild-type controls. Kidneys lacking HMGCS2 exhibited a decrease in ketone content and an increase in lipid droplet accumulation after IRI. Proximal tubular\u2013specific mitochondria lacking HMGCS2 had significantly lower fatty acid oxidation capacity both at baseline and after ischemic injury. Administration of a ketogenic diet for 4 days before IRI was sufficient to decrease kidney injury and augment mitochondrial fatty acid oxidation in kidney\n                      <jats:italic toggle=\"yes\">Hmgcs2<\/jats:italic>\n                      knockout mice. Kidney tissue lipidomics revealed that the loss of kidney HMGCS2 was associated with a decrease in both arachidonic acid containing phospholipids and prostaglandin levels.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Loss of renal HMGCS2 and resultant ketogenesis increased ischemia-induced injury and decreased mitochondrial fatty acid oxidation capacity, suggesting a role in renal ketogenesis in limiting AKI.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.0000001014","type":"journal-article","created":{"date-parts":[[2026,1,21]],"date-time":"2026-01-21T17:00:34Z","timestamp":1769014834000},"page":"1628-1642","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":7,"title":["Renal Ketogenesis Protects Against Ischemic Kidney 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Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0005-2392-5190","authenticated-orcid":false,"given":"Emma-Grace","family":"Haley","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine (Nephrology) and Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0780-1225","authenticated-orcid":false,"given":"Chetana","family":"Jadhav","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine (Nephrology) and Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas"},{"name":"Department of Cell Biology, University of Texas Southwestern Medical Center, Dallas, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-0954-610X","authenticated-orcid":false,"given":"Ricardo","family":"Monroy","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine (Nephrology) and Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tatyana","family":"McCoy","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine (Nephrology) and Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6420-2400","authenticated-orcid":false,"given":"Sarah C.","family":"Huen","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine (Nephrology) and Pharmacology, University of Texas Southwestern Medical Center, Dallas, 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