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Matrix metalloproteinases (MMPs) modulate inflammation and fibrosis by degrading a variety of extracellular matrix and regulating the activities of effector proteins. Abnormal regulation of MMP-12 expression has been implicated in abdominal aortic aneurysm, atherosclerosis and emphysema, but the underlying mechanisms remain unclear. The present study examined the function of MMP-12 in glomerular fibrogenesis and inflammation using <jats:italic>apo E<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> or <jats:italic>apo E<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup><jats:italic>MMP-12<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice and maintained on a high-fat-diet (HFD) for 3, 6, or 9 months. <jats:italic>MMP-12<\/jats:italic> deletion reduced glomerular matrix accumulation and downregulated the expression of NADPH oxidase 4 and the subunit-p67<jats:sup>phox<\/jats:sup>, indicating the inhibition of renal oxidative stress. In addition, the expression of the inflammation-associated molecule MCP-1 and macrophage marker-CD11b was decreased in glomeruli of <jats:italic>apo E<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup><jats:italic>MMP-12<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice fed HFD. MMP-12 produced by macrophages infiltrating into glomeruli contributed to the degradation of collagen type IV and fibronectin. Crescent formation due to renal oxidative stress in Bowman\u2019s space was a major factor in the development of fibrogenesis and inflammation. 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