{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T01:00:21Z","timestamp":1790816421933,"version":"4.1.0"},"reference-count":77,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2022,10,7]],"date-time":"2022-10-07T00:00:00Z","timestamp":1665100800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell Dev. Biol."],"abstract":"<jats:p>Cardiomyopathy is a myocardial disorder, in which the heart muscle is structurally and functionally abnormal, often leading to heart failure. Dilated cardiomyopathy is characterized by a compromised left ventricular function and contributes significantly to the heart failure epidemic, which represents a staggering clinical and public health problem worldwide. Gene mutations have been identified in 35% of patients with dilated cardiomyopathy. Pathogenic variants in <jats:italic>LMNA,<\/jats:italic> encoding nuclear A-type lamins, are one of the major causative causes of dilated cardiomyopathy (i.e. <jats:italic>CardioLaminopathy<\/jats:italic>). A-type lamins are type V intermediate filament proteins, which are the main components of the nuclear lamina. The nuclear lamina is connected to the cytoskeleton on one side, and to the chromatin on the other side. Among the models proposed to explain how <jats:italic>CardioLaminopathy<\/jats:italic> arises, the \u201cchromatin model\u201d posits an effect of mutated A-type lamins on the 3D genome organization and thus on the transcription activity of tissue-specific genes. Chromatin contacts with the nuclear lamina <jats:italic>via<\/jats:italic> specific genomic regions called lamina-associated domains lamina-associated domains. These LADs play a role in the chromatin organization and gene expression regulation. This review focuses on the identification of LADs and chromatin remodeling in cardiac muscle cells expressing mutated A-type lamins and discusses the methods and relevance of these findings in disease.<\/jats:p>","DOI":"10.3389\/fcell.2022.1030950","type":"journal-article","created":{"date-parts":[[2022,10,7]],"date-time":"2022-10-07T04:28:11Z","timestamp":1665116891000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":7,"title":["Genome organization in cardiomyocytes expressing mutated A-type lamins"],"prefix":"10.3389","volume":"10","author":[{"given":"Marie","family":"Kervella","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maureen","family":"Jahier","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Albano C.","family":"Meli","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antoine","family":"Muchir","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2022,10,7]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"610","DOI":"10.15252\/embr.201439789","article-title":"Nuclear lamins are not required for lamina\u2010associated domain organization in mouse embryonic stem cells","volume":"16","author":"Amendola","year":"2015","journal-title":"EMBO Rep."},{"key":"B2","doi-asserted-by":"publisher","first-page":"dev173666","DOI":"10.1242\/dev.173666","article-title":"DamID as a versatile tool for understanding gene regulation","volume":"146","author":"Aughey","year":"2019","journal-title":"Development"},{"key":"B3","doi-asserted-by":"publisher","first-page":"25","DOI":"10.1002\/wdev.205","article-title":"Dam it\u2019s good! 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