{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T00:01:47Z","timestamp":1788134507244,"version":"build-2803163510"},"reference-count":112,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2023,7,7]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Systemic defects in intestinal iron absorption, circulation, and retention cause iron deficiency in 50% of patients with heart failure. Defective subcellular iron uptake mechanisms that are independent of systemic absorption are incompletely understood. The main intracellular route for iron uptake in cardiomyocytes is clathrin-mediated endocytosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>\n                      We investigated subcellular iron uptake mechanisms in patient-derived and CRISPR\/Cas\u2013edited induced pluripotent stem cell\u2013derived cardiomyocytes as well as patient-derived heart tissue. We used an integrated platform of DIA-MA (mass spectrometry data-independent acquisition)\u2013based proteomics and signaling pathway interrogation. We employed a genetic induced pluripotent stem cell model of 2 inherited mutations (\n                      <jats:italic>TnT<\/jats:italic>\n                      [\n                      <jats:italic>troponin T<\/jats:italic>\n                      ]-R141W and\n                      <jats:italic>TPM1<\/jats:italic>\n                      [\n                      <jats:italic>tropomyosin 1<\/jats:italic>\n                      ]-L185F) that lead to dilated cardiomyopathy (DCM), a frequent cause of heart failure, to study the underlying molecular dysfunctions of DCM mutations.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      We identified a druggable molecular pathomechanism of impaired subcellular iron deficiency that is independent of systemic iron metabolism. Clathrin-mediated endocytosis defects as well as impaired endosome distribution and cargo transfer were identified as a basis for subcellular iron deficiency in DCM-induced pluripotent stem cell\u2013derived cardiomyocytes. The clathrin-mediated endocytosis defects were also confirmed in the hearts of patients with DCM with end-stage heart failure. Correction of the\n                      <jats:italic>TPM1-L185F<\/jats:italic>\n                      mutation in DCM patient\u2013derived induced pluripotent stem cells, treatment with a peptide, Rho activator II, or iron supplementation rescued the molecular disease pathway and recovered contractility. Phenocopying the effects of the\n                      <jats:italic>TPM1-L185F<\/jats:italic>\n                      mutation into WT induced pluripotent stem cell\u2013derived cardiomyocytes could be ameliorated by iron supplementation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>Our findings suggest that impaired endocytosis and cargo transport resulting in subcellular iron deficiency could be a relevant pathomechanism for patients with DCM carrying inherited mutations. Insight into this molecular mechanism may contribute to the development of treatment strategies and risk management in heart failure.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circresaha.122.321157","type":"journal-article","created":{"date-parts":[[2023,6,14]],"date-time":"2023-06-14T05:00:16Z","timestamp":1686718816000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":13,"title":["An Alternative Mechanism of Subcellular Iron Uptake Deficiency in Cardiomyocytes"],"prefix":"10.1161","volume":"133","author":[{"given":"Yuanyuan","family":"Dai","sequence":"first","affiliation":[{"name":"Heart Research Center Goettingen, Clinic for Cardiology and Pneumology, University Medical Center Goettingen, Georg-August University of Goettingen, Germany (Y.D., N.I., H.X., R.W., K.T., S.B., S.S., E.M.Z., S.E.L., G.H., A.E.)."},{"name":"DZHK (German Center for Cardiovascular Research), partner site Goettingen, Germany (Y.D., N.I., H.X., R.W., K.T., S.B., C.L., J.P., F.E.F., E.M.Z., I.K., N.V., S.E.L., G.H., A.E.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nadezda","family":"Ignatyeva","sequence":"additional","affiliation":[{"name":"Heart Research Center Goettingen, Clinic for Cardiology and Pneumology, University Medical Center Goettingen, Georg-August University of Goettingen, Germany (Y.D., N.I., H.X., R.W., K.T., S.B., S.S., E.M.Z., S.E.L., G.H., A.E.)."},{"name":"DZHK (German Center for Cardiovascular Research), partner site Goettingen, Germany (Y.D., N.I., H.X., R.W., K.T., S.B., C.L., J.P., F.E.F., E.M.Z., I.K., N.V., S.E.L., G.H., A.E.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hang","family":"Xu","sequence":"additional","affiliation":[{"name":"Heart Research Center Goettingen, Clinic for Cardiology and Pneumology, University Medical Center Goettingen, Georg-August University of Goettingen, Germany (Y.D., N.I., H.X., R.W., K.T., S.B., S.S., E.M.Z., S.E.L., G.H., A.E.)."},{"name":"DZHK (German Center for Cardiovascular Research), partner site Goettingen, Germany (Y.D., N.I., H.X., R.W., K.T., S.B., C.L., J.P., F.E.F., E.M.Z., I.K., N.V., S.E.L., G.H., A.E.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruheen","family":"Wali","sequence":"additional","affiliation":[{"name":"Heart Research Center Goettingen, Clinic for Cardiology and Pneumology, University Medical Center Goettingen, Georg-August University of Goettingen, Germany (Y.D., N.I., H.X., R.W., K.T., S.B., S.S., E.M.Z., S.E.L., G.H., A.E.)."},{"name":"DZHK (German Center for Cardiovascular Research), partner site Goettingen, Germany (Y.D., N.I., H.X., R.W., K.T., S.B., C.L., J.P., F.E.F., E.M.Z., I.K., N.V., S.E.L., G.H., A.E.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karl","family":"Toischer","sequence":"additional","affiliation":[{"name":"Heart Research Center Goettingen, Clinic for Cardiology and Pneumology, University Medical 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