MiR-30c/PGC-1β protects against diabetic cardiomyopathy via PPARα View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-12

AUTHORS

Zhongwei Yin, Yanru Zhao, Mengying He, Huaping Li, Jiahui Fan, Xiang Nie, Mengwen Yan, Chen Chen, Dao Wen Wang

ABSTRACT

BACKGROUND: Metabolic abnormalities have been implicated as a causal event in diabetic cardiomyopathy (DCM). However, the mechanisms underlying cardiac metabolic disorder in DCM were not fully understood. RESULTS: Db/db mice, palmitate treated H9c2 cells and primary neonatal rat cardiomyocytes were employed in the current study. Microarray data analysis revealed that PGC-1β may play an important role in DCM. Downregulation of PGC-1β relieved palmitate induced cardiac metabolism shift to fatty acids use and relevant lipotoxicity in vitro. Bioinformatics coupled with biochemical validation was used to confirm that PGC-1β was one of the direct targets of miR-30c. Remarkably, overexpression of miR-30c by rAAV system improved glucose utilization, reduced excessive reactive oxygen species production and myocardial lipid accumulation, and subsequently attenuated cardiomyocyte apoptosis and cardiac dysfunction in db/db mice. Similar effects were also observed in cultured cells. More importantly, miR-30c overexpression as well as PGC-1β knockdown reduced the transcriptional activity of PPARα, and the effects of miR-30c on PPARα was almost abated by PGC-1β knockdown. CONCLUSIONS: Our data demonstrated a protective role of miR-30c in cardiac metabolism in diabetes via targeting PGC-1β, and suggested that modulation of PGC-1β by miR-30c may provide a therapeutic approach for DCM. More... »

PAGES

7

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1186/s12933-019-0811-7

    DOI

    http://dx.doi.org/10.1186/s12933-019-0811-7

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1111363536

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30635067


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