Abstract:In response to hypertensive stimuli, like angiotensin II (AngII), cardiac fibroblasts (CFs) transform into an activated phenotype, which triggers increased collagen deposition and pro‐inflammatory signals. Transforming growth factor beta 1 (TGF‐β1) and reactive oxygen species are important modulators of AngII‐induced cardiac fibrosis and CF activation. The extent to which the AngII‐induced changes in CF phenotype persist in the absence of ongoing stimulation is not known. The objective of the present study was… Show more
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