| Literature DB >> 33339579 |
M Pilar Bayona-Bafaluy1, Eldris Iglesias2, Ester López-Gallardo3, Sonia Emperador4, David Pacheu-Grau5, Lorenzo Labarta6, Julio Montoya7, Eduardo Ruiz-Pesini8.
Abstract
Dilated cardiomyopathy is a frequent and extremely heterogeneous medical condition. Deficits in the oxidative phosphorylation system have been described in patients suffering from dilated cardiomyopathy. Hence, mutations in proteins related to this biochemical pathway could be etiological factors for some of these patients. Here, we review the clinical phenotypes of patients harboring pathological mutations in genes related to the oxidative phosphorylation system, either encoded in the mitochondrial or in the nuclear genome, presenting with dilated cardiomyopathy. In addition to the clinical heterogeneity of these patients, the large genetic heterogeneity has contributed to an improper allocation of pathogenicity for many candidate mutations. We suggest criteria to avoid incorrect assignment of pathogenicity to newly found mutations and discuss possible therapies targeting the oxidative phosphorylation function.Entities:
Keywords: Dilated cardiomyopathy; Mitochondrial DNA; Mitochondrial biogenesis; Oxidative phosphorylation; Pathogenicity criteria; Pathologic mutation
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Year: 2020 PMID: 33339579 DOI: 10.1016/j.mrrev.2020.108334
Source DB: PubMed Journal: Mutat Res Rev Mutat Res ISSN: 1383-5742 Impact factor: 5.657