GRK5 is a regulator of fibroblast activation and cardiac fibrosis | Zendy

Akito Eguchi | Zendy; Ryan C. Coleman | Zendy; Kenneth S. Gresham | Zendy; Erhe Gao | Zendy; Jessica Ibetti | Zendy; J. Kurt Chuprun | Zendy; Walter J. Koch | Zendy

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GRK5 is a regulator of fibroblast activation and cardiac fibrosis

Author(s) -

Akito Eguchi,

Ryan C. Coleman,

Kenneth S. Gresham,

Erhe Gao,

Jessica Ibetti,

J. Kurt Chuprun,

Walter J. Koch

Publication year - 2021

Publication title -

proceedings of the national academy of sciences

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 5.011

H-Index - 771

eISSN - 1091-6490

pISSN - 0027-8424

DOI - 10.1073/pnas.2012854118

Subject(s) - nfat , cardiac fibrosis , fibroblast , angiotensin ii , biology , fibrosis , microbiology and biotechnology , heart failure , endocrinology , medicine , cancer research , receptor , transcription factor , in vitro , biochemistry , gene

Significance Pathological remodeling of the heart is a hallmark of chronic heart failure (HF) and these structural changes further perpetuate the disease. G protein-coupled receptor (GPCR) kinase 5 (GRK5) has been shown to cause deleterious effects on the cardiomyocyte during HF; however, its effects in cardiac fibroblasts, the crucial cell type responsible for maintaining the structural integrity of the heart, is not understood. Here, we use in vitro and in vivo methods to demonstrate that inhibition of GRK5 inhibits fibroblast activation and attenuates the fibrotic response in the heart.

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