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Population
Angiotensin II-stimulated cardiac fibroblasts
Design
In vitro laboratory study
Hypothesis-generating for antifibrotic targets; extends fibroblast collagen mechanisms but leaves clinical translation open.
channel, transient receptor potential cation channel subfamily C member 6 (TRPC6), and the profibrotic transcription factor, Yes-associated protein (YAP). This finding indicated that fibroblast-to-myofibroblast conversion is mechanistically coupled to collagen expression. The observation that collagen receptor cross-talk underlies α-SMA-dependent collagen type I expression in cardiac fibroblasts expands our understanding of the complex mechanisms involved in collagen gene expression in the heart and may be relevant to cardiac fibrogenesis.
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Venugopal et al. (2019) studied this question.
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