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people with type 2 diabetes and correlates with podocyte loss.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>AdipoR1 knockout induced glomerular injury and fibrosis in mice, predominantly in males.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            AdipoR1 knockdown podocytes showed impaired trafficking of active integrin\n                            <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                            1, fibronectin accumulation, impaired adhesion, and increased apoptosis.\n                          <\/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>Deficiency of adiponectin and its downstream signaling may contribute to the pathogenesis of kidney injury in type 2 diabetes. Adiponectin activates intracellular signaling using adiponectin receptor 1 (AdipoR1) and adiponectin receptor 2, but the role of adiponectin receptor\u2013mediated signaling in glomerular injury in type 2 diabetes remains unknown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>The expression of AdipoR1 in the kidneys of people with type 2 diabetes and the expression of podocyte proteins or injury markers in the kidneys of AdipoR1 knockout (AdipoR1-KO) mice and immortalized AdipoR1-deficient human podocytes were investigated by immunohistochemistry and immunoblotting. The functional role of AdipoR1 was studied in AdipoR1-deficient podocytes by performing assays for apoptosis, cytokine secretion, mechanical stress, adhesion, and endocytic trafficking.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Glomerular AdipoR1 expression was lower in type 2 diabetes and associated kidney disease, correlating with higher body mass index and podocyte loss. Male AdipoR1-KO mice showed typical signs of early diabetic kidney disease, including albuminuria, glomerular structural abnormalities, and lower expression of central podocyte proteins; females were less affected. Podocyte apoptosis increased in female and male AdipoR1-KO mice, and excessive podocyte loss, potentially due to detachment, was detected in males. AdipoR1 deficiency impaired the yes-associated protein\u2013mediated mechanoresponse and induced accumulation of the extracellular matrix (ECM) protein fibronectin in the glomeruli\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      and podocytes\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      . Functionally, AdipoR1 deficiency impaired endocytosis of the ECM receptor active integrin\n                      <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                      1, disturbed focal adhesion turnover, and remodulated podocyte-derived ECM, thereby reducing podocyte adhesion.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      AdipoR1 deficiency in mice resulted in the development of kidney injury predominantly in males. Mechanistically, AdipoR1 loss in podocytes impaired endocytosis of active integrin\n                      <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                      1, which plausibly compromised focal adhesion dynamics, disturbed fibronectin matrix turnover, and hindered podocyte adhesion.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.0000000611","type":"journal-article","created":{"date-parts":[[2025,1,28]],"date-time":"2025-01-28T12:04:37Z","timestamp":1738065877000},"page":"825-844","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":3,"title":["Integrin Trafficking, Fibronectin Architecture, and Glomerular Injury upon Adiponectin Receptor 1 Depletion"],"prefix":"10.1681","volume":"36","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2024-0760","authenticated-orcid":false,"given":"Sonja","family":"Lindfors","sequence":"first","affiliation":[{"name":"Research Program 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