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Knockdown of MFRN1 enhances HMOX2 ubiquitination by MITOL

Effects of inorganic arsenic on human prostate stem-progenitor cell transformation, autophagic flux blockade, and NRF2 pathway activation

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Because typical early atherosclerotic lesion formation observed in hyperhomocysteinemic animals can be prevented by an antiplatelet therapy with dipyridamole, the authors concluded that platelet-mediated proliferation of smooth muscle cells is a potential cellular mechanism involved in the atherogenicity of hyperhomocysteinemia