{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T20:02:06Z","timestamp":1791316926542,"version":"4.3.1"},"reference-count":81,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","license":[{"start":{"date-parts":[[2026,4,24]],"date-time":"2026-04-24T00:00:00Z","timestamp":1776988800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2026,4,24]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Cardiomyocyte mitochondria align with sarcomeres during heart development. Mitochondrial motility is controlled by RHOT (ras homolog family member T) 1 and RHOT2. RHOT1 and RHOT2 are atypical Rho-like small GTPases that are anchored to the outer mitochondrial membrane and couple mitochondria to kinesin and dynein motors. We hypothesized that RHOT protein expression and mitochondrial motility are required for mitochondrial positioning during cardiomyocyte development.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      We generated mice with cardiomyocyte-selective deletion of\n                      <jats:italic toggle=\"yes\">Rhot1<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">Rhot2<\/jats:italic>\n                      during embryogenesis (cRhot1\/2-KO [constitutive and embryonic cardiomyocyte-selective\n                      <jats:italic toggle=\"yes\">Rhot1<\/jats:italic>\n                      \/2 knockout]) or tamoxifen-inducible deletion in the adult heart (iRhot1\/2-KO [inducible cardiomyocyte-selective\n                      <jats:italic toggle=\"yes\">Rhot1\/2<\/jats:italic>\n                      knockout]) to assess the importance of mitochondrial motility during and after cardiomyocyte maturation. Mitochondrial motility was determined by a motor protein\u2013driven single mitochondria motility assay. Respiratory capacity was measured in isolated mitochondria. Intracellular mitochondrial localization and ATP production in isolated cardiomyocytes were assessed by confocal microscopy and after adenoviral expression of the fluorescence resonance energy transfer\u2013based ATP biosensor ATeam. Cardiac ultrastructure was assessed by electron micrographs; mass spectrometry was used for proteome analysis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      cRhot1\/2-KO mice developed fatal cardiomyopathy associated with sarcomere disarray and perinuclear accumulation of mitochondria and ATP production. Mitochondria isolated from cRhot1\/2-KO hearts exhibited impaired motility but preserved respiratory capacity. Mechanistically, proteome analysis identified that RHOT proteins bind mitochondria to contractile muscle fiber proteins. In contrast, inducible deletion of\n                      <jats:italic toggle=\"yes\">Rhot1<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">Rhot2<\/jats:italic>\n                      in adult iRhot1\/2-KO mice did not result in heart failure. Despite impaired motility of isolated mitochondria, intracellular mitochondrial localization, local ATP production, and sarcomere structure were preserved in adult iRhot1\/2-KO hearts after cardiomyocyte maturation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>RHOT proteins bind mitochondria to contractile muscle fiber proteins and are required for mitochondrial positioning in cardiomyocytes during development. Our study links mitochondrial motility and local ATP production to structural and functional maturation of the heart.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circresaha.125.327297","type":"journal-article","created":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T09:00:43Z","timestamp":1773651643000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":3,"title":["RHOT Proteins Link Mitochondrial Motility to Cardiomyocyte Sarcomere Maturation"],"prefix":"10.1161","volume":"138","author":[{"given":"Natali","family":"Froese","sequence":"first","affiliation":[{"name":"Department of Cardiology and Angiology (N.F., I.S., F.P., J.J., M.K.-K., P.G., A.G., K.W., S.E., M.H., M.S., M.R.-H., K.C.W., J.B., C.R.), Hannover Medical School, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-8513-1606","authenticated-orcid":true,"given":"Ivanna","family":"Shymotiuk","sequence":"additional","affiliation":[{"name":"Department of Cardiology and Angiology (N.F., I.S., F.P., J.J., M.K.-K., P.G., A.G., K.W., S.E., M.H., M.S., M.R.-H., K.C.W., J.B., C.R.), Hannover Medical School, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander","family":"Froese","sequence":"additional","affiliation":[{"name":"Institute of Experimental Cardiovascular Research, University Medical Center Hamburg-Eppendorf, Germany (A.F., V.O.N.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1076-5272","authenticated-orcid":true,"given":"Felix","family":"Polten","sequence":"additional","affiliation":[{"name":"Department of Cardiology and Angiology (N.F., I.S., F.P., J.J., M.K.-K., P.G., A.G., K.W., S.E., M.H., M.S., M.R.-H., K.C.W., J.B., C.R.), Hannover Medical School, Germany."},{"name":"Division of Molecular and Translational Cardiology (F.P., M.K.-K., K.C.W.), Hannover Medical School, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonas","family":"Jablinski","sequence":"additional","affiliation":[{"name":"Department of Cardiology and Angiology (N.F., I.S., F.P., J.J., M.K.-K., P.G., A.G., K.W., S.E., M.H., M.S., M.R.-H., K.C.W., J.B., C.R.), Hannover Medical School, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2127-9843","authenticated-orcid":true,"given":"Tim","family":"Scholz","sequence":"additional","affiliation":[{"name":"Institute of Molecular and Cell Physiology (T. 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