Macrophage mitochondrial-derived reactive oxygen species (mtROS) enhances early atherosclerogenesis
نویسندگان
چکیده
Excessive accumulation of mitochondrial-derived reactive oxygen species (mtROS) occurs in different types of cells in the atherosclerotic lesions of both humans and animal models. However, evidences on the causative roles of myeloid cell specific mtROS in atherosclerosis are limited. Mechanistically, lesional factors that stimulate mtROS remain to be determined, and the potential pathogenic intracellular signals require further investigation. We have recently provided new evidences that arteriosclerotic lesions, monocyte infiltration-associated chronic inflammation are enhanced by mtROS accumulation in lesional macrophages. Additionally, our study has revealed an important signaling pathway linking mtROS to the activation of an essential transcription factor NF-кB (RelA) and its downstream chemokine MCP-1. This pathway drives monocyte infiltration and amplifies the chronic inflammation during the early atherosclerogenesis.
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