{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T13:24:19Z","timestamp":1790688259055,"version":"4.1.0"},"reference-count":53,"publisher":"American Society for Clinical Investigation","issue":"13","funder":[{"DOI":"10.13039\/501100001809","name":"the National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["8163066"],"award-info":[{"award-number":["8163066"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100001809","name":"the National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["81870532"],"award-info":[{"award-number":["81870532"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"name":"the Guangdong Provincial Science and Technology Innovation Council Grant","award":["2017B030301018"],"award-info":[{"award-number":["2017B030301018"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,7,11]]},"abstract":"<jats:p>\n                    Kindlin-2 regulates integrin-mediated cell adhesion to and migration on the extracellular matrix. Our recent studies demonstrate important roles of kindlin-2 in regulation of mesenchymal stem cell differentiation and skeletal development. In this study, we generated adipose tissue\u2013specific conditional knockout of kindlin-2 in mice by using\n                    <jats:italic>Adipoq-Cre<\/jats:italic>\n                    BAC\u2013transgenic mice. The results showed that deleting kindlin-2 expression in adipocytes in mice caused a severe lipodystrophy with drastically reduced adipose tissue mass. Kindlin-2 ablation elevated the blood levels of nonesterified fatty acids and triglycerides, resulting in massive fatty livers in the mutant mice fed with high-fat diet (HFD). Furthermore, HFD-fed mutant mice displayed type II diabetes\u2013like phenotypes, including elevated levels of fasting blood glucose, glucose intolerance, and peripheral insulin resistance. Kindlin-2 loss dramatically reduced the expression levels of multiple key factors, including PPAR\u03b3, mTOR, AKT, and \u03b2-catenin proteins, and suppressed adipocyte gene expression and differentiation. Finally, kindlin-2 loss drastically reduced leptin production and caused a high bone mass phenotype. Collectively, these studies establish a critical role of kindlin-2 in control of adipogenesis and lipid metabolism as well as bone homeostasis.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.128405","type":"journal-article","created":{"date-parts":[[2019,7,10]],"date-time":"2019-07-10T11:02:24Z","timestamp":1562756544000},"source":"Crossref","is-referenced-by-count":53,"title":["Lipoatrophy and metabolic disturbance in mice with adipose-specific deletion of kindlin-2"],"prefix":"10.1172","volume":"4","author":[{"given":"Huanqing","family":"Gao","sequence":"first","affiliation":[{"name":"Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, and Department of Biology, Southern University of Science and Technology, Shenzhen, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuxi","family":"Guo","sequence":"additional","affiliation":[{"name":"Guangdong Provincial Key Laboratory 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