{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T14:44:00Z","timestamp":1792421040782,"version":"4.5.0"},"reference-count":60,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2015,8,14]]},"abstract":"<jats:sec>\n            <jats:title>\n              <jats:underline>Rationale:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>\n              Skeletal muscle wasting with accompanying cachexia is a life threatening complication in congestive heart failure. The molecular mechanisms are imperfectly understood, although an activated renin\u2013angiotensin aldosterone system has been implicated. Angiotensin (Ang) II induces skeletal muscle atrophy in part by increased muscle-enriched E3 ubiquitin ligase muscle RING-finger-1 (\n              <jats:italic>MuRF1<\/jats:italic>\n              ) expression, which may involve protein kinase D1 (PKD1).\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Objective:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>To elucidate the molecular mechanism of Ang II\u2013induced skeletal muscle wasting.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Methods and Results:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>\n              A cDNA expression screen identified the lysosomal hydrolase-coordinating transcription factor EB (TFEB) as novel regulator of the human\n              <jats:italic>MuRF1<\/jats:italic>\n              promoter. TFEB played a key role in regulating Ang II\u2013induced skeletal muscle atrophy by transcriptional control of\n              <jats:italic>MuRF1<\/jats:italic>\n              via conserved E-box elements. Inhibiting TFEB with small interfering RNA prevented Ang II\u2013induced\n              <jats:italic>MuRF1<\/jats:italic>\n              expression and atrophy. The histone deacetylase-5 (HDAC5), which was directly bound to and colocalized with TFEB, inhibited TFEB-induced\n              <jats:italic>MuRF1<\/jats:italic>\n              expression. The inhibition of TFEB by HDAC5 was reversed by PKD1, which was associated with HDAC5 and mediated its nuclear export. Mice lacking PKD1 in skeletal myocytes were resistant to Ang II\u2013induced muscle wasting.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Conclusion:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>We propose that elevated Ang II serum concentrations, as occur in patients with congestive heart failure, could activate the PKD1\/HDAC5\/TFEB\/MuRF1 pathway to induce skeletal muscle wasting.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circresaha.114.305393","type":"journal-article","created":{"date-parts":[[2015,8,13]],"date-time":"2015-08-13T20:18:22Z","timestamp":1439497102000},"page":"424-436","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":91,"title":["Angiotensin II Induces Skeletal Muscle Atrophy by Activating TFEB-Mediated\n            <i>MuRF1<\/i>\n            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Germany (P.D.B., C.P.T., D.L., M.K., F.S., S.S., J.F.); Department of Cardiology, Charit\u00e9 Universit\u00e4tsmedizin Berlin, Campus Virchow, Berlin, Germany (J.F.); and Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas (K.S., R.B.-D., E.N.O.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Doerte","family":"Lodka","sequence":"additional","affiliation":[{"name":"From the Department of Molecular Cardiology, Experimental and Clinical Research Center (ECRC), a Cooperation between Max-Delbr\u00fcck-Centrum and Charit\u00e9 Universit\u00e4tsmedizin Berlin, Campus Buch, Berlin, Germany (P.D.B., C.P.T., D.L., M.K., F.S., S.S., J.F.); Department of Cardiology, Charit\u00e9 Universit\u00e4tsmedizin Berlin, Campus Virchow, Berlin, Germany (J.F.); and Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas (K.S., R.B.-D., 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Berlin, Germany (P.D.B., C.P.T., D.L., M.K., F.S., S.S., J.F.); Department of Cardiology, Charit\u00e9 Universit\u00e4tsmedizin Berlin, Campus Virchow, Berlin, Germany (J.F.); and Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas (K.S., R.B.-D., E.N.O.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kunhua","family":"Song","sequence":"additional","affiliation":[{"name":"From the Department of Molecular Cardiology, Experimental and Clinical Research Center (ECRC), a Cooperation between Max-Delbr\u00fcck-Centrum and Charit\u00e9 Universit\u00e4tsmedizin Berlin, Campus Buch, Berlin, Germany (P.D.B., C.P.T., D.L., M.K., F.S., S.S., J.F.); Department of Cardiology, Charit\u00e9 Universit\u00e4tsmedizin Berlin, Campus Virchow, Berlin, Germany (J.F.); and Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas (K.S., R.B.-D., 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