Ablation of lysophosphatidic acid receptor 1 attenuates hypertrophic cardiomyopathy in a mouse model.

ABSTRACT: Myocardial fibrosis is a key pathologic feature of hypertrophic cardiomyopathy (HCM). However, the fibrotic pathways activated by HCM-causing sarcomere protein gene mutations are poorly defined. Because lysophosphatidic acid is a mediator of fibrosis in multiple organs and diseases, we tested the role of the lysophosphatidic acid pathway in HCM. Lysphosphatidic acid receptor 1 (LPAR1), a cell surface receptor, is required for lysophosphatidic acid mediation of fibrosis. We bred HCM mice carrying a pathogenic myosin heavy-chain variant (403^+/-) with Lpar1-ablated mice to create mice carrying both genetic changes (403^+/- LPAR1 ^-/-) and assessed development of cardiac hypertrophy and fibrosis. Compared with 403^+/- LPAR1^WT, 403

SUBMITTER: Axelsson Raja A 

PROVIDER: S-EPMC9282378 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature