https://www.selleckchem.com/products/ABT-888.html
Furthermore, Mep1A was expressed mainly in MCs, wherein it mediated TNF-α expression. Mep1A inhibitor actinonin significantly inhibited TNF-α secretion in MCs. TNF-α secreted by MCs enhanced MMP2 expression in SMCs and promoted SMC apoptosis. CONCLUSION AND IMPLICATIONS Taken together, these data suggest that Mep1A may be vital in AAA pathophysiology by regulating TNF-α production by MCs. Knocking out Mep1A significantly decreased AAA diameter and improved AAA stability in mice. Therefore, Mep1A is a potential new therapeutic target in
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