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RAAS inhibitors are cornerstone therapies for hypertension, heart failure, and post-myocardial infarction, with both systemic and local cardiac effects contributing to inflammation and fibrosis
doi:10.1016/S0167-4838(01)00181-9 39
Mechanistically, aloxistatin attenuated TGF1-induced pro-fibrotic signaling in cardiomyopathy-derived HCFs by inhibiting extracellular matrix organization-related gene expression and secretion of MMP2 und FN1, partially mediated through CAPN2 inhibition
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[3] [4] GLP-1 and GIP receptor activation promotes insulin secretion in a glucose-dependent manner and contributes to appetite suppression
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