{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T08:35:00Z","timestamp":1793349300533,"version":"4.5.0"},"reference-count":43,"publisher":"Oxford University Press (OUP)","issue":"13","license":[{"start":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T00:00:00Z","timestamp":1784592000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/501100001665","name":"French National Research Agency","doi-asserted-by":"publisher","award":["ANR-19-CE17-0013-02"],"award-info":[{"award-number":["ANR-19-CE17-0013-02"]}],"id":[{"id":"10.13039\/501100001665","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002915","name":"Fondation pour la Recherche M\u00e9dicale","doi-asserted-by":"publisher","award":["FDT202304016874"],"award-info":[{"award-number":["FDT202304016874"]}],"id":[{"id":"10.13039\/501100002915","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001674","name":"Leducq Foundation","doi-asserted-by":"publisher","award":["18CVD05"],"award-info":[{"award-number":["18CVD05"]}],"id":[{"id":"10.13039\/501100001674","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,9,24]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Mutations in the LMNA gene, which encodes lamin A\/C, cause a variety of diseases known as laminopathies. Some mutations are particularly associated with the occurrence of dilated cardiomyopathy and heart failure, but the genotype\u2013phenotype relationship and underlying mechanisms are unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>Induced pluripotent stem cells (hiPSCs) from a patient carrying a LMNA point mutation (c.665A&amp;gt;C, p.His222Pro) and a CRISPR\/Cas9 corrected isogenic control hiPSC clones were differentiated into cardiomyocytes (hiPSC-CMs), with no difference in the differentiation yield and in sarcomere organization between the two cell lines. However, 3D cardiac organoids generated with LMNA p.H222P hiPSC-CMs showed an impaired contractility compared to control organoids. Calcium transient recordings in LMNA p.H222P mutant cardiomyocytes showed a significantly higher calcium transient amplitude with a significantly slower calcium reuptake. Transcriptomic analyses suggested a global mitochondrial dysfunction and in particular an impaired mitochondrial calcium uptake with a significantly decreased expression of the mitochondrial calcium uniporter (MCU). This decrease in MCU expression was confirmed by western blot and was accompanied by an increased MICU1:MCU ratio, as well as an increased PDH Ser232 and PDH Ser300 phosphorylation, indicating an altered mitochondrial calcium uptake in the LMNA mutant hiPSC-CMs. Consistently, lower mitochondrial respiration and ATP levels were found in LMNA p.H222P hiPSC-CMs as compared to isogenic controls. Strikingly, treatment with the MCU activator amorolfine restored mitochondrial calcium uptake and improved contractility in LMNA mutant hiPSC-CMs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our results establish a direct mechanistic link between nuclear envelope dysfunction and impaired mitochondrial function and highlight the MCU complex as a potential therapeutic target in LMNA-related cardiomyopathy. More broadly, this work provides a paradigm for connecting gene-specific nuclear defects to mitochondrial dysfunction in inherited cardiomyopathies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cvr\/cvag163","type":"journal-article","created":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T13:20:54Z","timestamp":1784640054000},"page":"1819-1833","source":"Crossref","is-referenced-by-count":2,"title":["<i>LMNA<\/i>\n                    p.H222P mutation causes contractile dysfunction via impaired mitochondrial calcium uptake in human cardiac laminopathy"],"prefix":"10.1093","volume":"122","author":[{"given":"Magali","family":"Seguret","sequence":"first","affiliation":[{"name":"INSERM, Universit\u00e9 de Paris Cit\u00e9, PARCC , 56 Rue Leblanc, Paris F-75015 ,","place":["France"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charl\u00e8ne","family":"Jouve","sequence":"additional","affiliation":[{"name":"INSERM, Universit\u00e9 de Paris Cit\u00e9, PARCC 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