期刊论文、会议论文

英文

Journal of Molecular and Cellular Cardiology

0022-2828

2020

140

SUPPL-S

55-55

ISHR World Congress

2019

Beijing, PEOPLES R CHINA

ISHR

THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND

ELSEVIER SCI LTD

10.1016/j.yjmcc.2019.11.133

National Heart, Lung, and Blood Institute at the NIHUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Heart Lung & Blood Institute (NHLBI) [1R01HL132182-01, R01 HL124248]; American Heart AssociationAmerican Heart Association [16GRNT30680004]; American Heart Association Career Development AwardAmerican Heart Association [18CDA34080244]; NATIONAL HEART, LUNG, AND BLOOD INSTITUTEUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Heart Lung & Blood Institute (NHLBI) [R01HL142097, R01HL132182, R01HL132182, R01HL124248, R01HL124248, R01HL142097, R01HL132182, R01HL124248, R01HL132182, R01HL132182] Funding Source: NIH RePORTER

本校为其他机构

Mutations in the BSCL2 gene underlie human type 2 Berardinelli-Seip congenital lipodystrophy (BSCL2) disease. Global Bscl2(-/-) mice recapitulate human BSCL2 lipodystrophy and results in the development of insulin resistance and hypertrophic cardiomyopathy. The pathological mechanisms underlying the development of lipodystrophy and cardiomyopathy in BSCL2 are controversial. Here we report that Bscl2(-/-) mice develop cardiac hypertrophy because of increased basal IGF1 receptor-mediated (IGF1R-mediated) PI3K/AKT signaling. Bscl2(-/-) hearts exhibited increased adipose triglyceride lipase (ATGL)...