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In contrast, mitochondria in liver cells have fewer cristae than muscle cells, as their energy requirements are not as extreme

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however, previous studies done on liver fibrosis and cardiac fibrosis in vivo and in vitro demonstrated that VCN was able to reduce the accumulation of fibrotic components possibly through its main pharmacological mechanism by targeting the PDE1A, where the latter has been identified as a key regulator of fibroblast activation and ECM remodeling in the heart 87