{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,20]],"date-time":"2026-06-20T05:19:57Z","timestamp":1781932797834,"version":"3.54.5"},"reference-count":51,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2017,8,2]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              The kidney is easily affected by aging\u2010associated changes, including glomerulosclerosis, tubular atrophy, and interstitial fibrosis. Particularly, renal tubulointerstitial fibrosis is a final common pathway in most forms of progressive renal disease. Angiotensin\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              type 1 receptor (\n              <jats:styled-content style=\"fixed-case\">AT<\/jats:styled-content>\n              1R)\u2010associated protein (\n              <jats:styled-content style=\"fixed-case\">ATRAP<\/jats:styled-content>\n              ), which was originally identified as a molecule that binds to\n              <jats:styled-content style=\"fixed-case\">AT<\/jats:styled-content>\n              1R, is highly expressed in the kidney. Previously, we have shown that\n              <jats:styled-content style=\"fixed-case\">ATRAP<\/jats:styled-content>\n              suppresses hyperactivation of\n              <jats:styled-content style=\"fixed-case\">AT<\/jats:styled-content>\n              1R signaling, but does not affect physiological\n              <jats:styled-content style=\"fixed-case\">AT<\/jats:styled-content>\n              1R signaling.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              We hypothesized that\n              <jats:styled-content style=\"fixed-case\">ATRAP<\/jats:styled-content>\n              has a novel functional role in the physiological age\u2010degenerative process, independent of modulation of\n              <jats:styled-content style=\"fixed-case\">AT<\/jats:styled-content>\n              1R signaling.\n              <jats:styled-content style=\"fixed-case\">ATRAP<\/jats:styled-content>\n              \u2010knockout mice were used to study the functional involvement of\n              <jats:styled-content style=\"fixed-case\">ATRAP<\/jats:styled-content>\n              in the aging.\n              <jats:styled-content style=\"fixed-case\">ATRAP<\/jats:styled-content>\n              \u2010knockout mice exhibit a normal age\u2010associated appearance without any evident alterations in physiological parameters, including blood pressure and cardiovascular and metabolic phenotypes. However, in\n              <jats:styled-content style=\"fixed-case\">ATRAP<\/jats:styled-content>\n              \u2010knockout mice compared with wild\u2010type mice, the following takes place: (1) age\u2010associated renal function decline and tubulointerstitial fibrosis are more enhanced; (2) renal tubular mitochondrial abnormalities and subsequent increases in the production of reactive oxygen species are more advanced; and (3) life span is 18.4% shorter (median life span, 100.4\u00a0versus 123.1\u00a0weeks). As a key mechanism, age\u2010related pathological changes in the kidney of\n              <jats:styled-content style=\"fixed-case\">ATRAP<\/jats:styled-content>\n              \u2010knockout mice correlated with decreased expression of the prosurvival gene,\n              <jats:italic>Sirtuin1<\/jats:italic>\n              . On the other hand, chronic angiotensin\n              <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n              infusion did not affect renal sirtuin1 expression in wild\u2010type mice.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              These results indicate that\n              <jats:styled-content style=\"fixed-case\">ATRAP<\/jats:styled-content>\n              plays an important role in inhibiting kidney aging, possibly through sirtuin1\u2010mediated mechanism independent of blocking\n              <jats:styled-content style=\"fixed-case\">AT<\/jats:styled-content>\n              1R signaling, and further protecting normal life span.\n            <\/jats:p>\n          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