Inflammation, Endoplasmic Reticulum Stress, Autophagy, and the Monocyte Chemoattractant Protein-1/CCR2 Pathway

    Authors

    P. E. Kolattukudy;J. L. Niu

    Comments

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    Abbreviated Journal Title

    Circ.Res.

    Keywords

    cardiovascular disease; type 2 diabetes; angiogenesis; adipogenesis; osteoclastogenesis; NF-KAPPA-B; PATTERN-RECOGNITION RECEPTORS; ZINC-FINGER PROTEIN; TOLL-LIKE RECEPTORS; C-REACTIVE PROTEIN; EXPERIMENTAL; MYOCARDIAL-INFARCTION; CARDIAC-SPECIFIC EXPRESSION; INSULIN-RESISTANCE; TRANSCRIPTION FACTOR; CARDIOVASCULAR-DISEASE; Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular; Disease

    Abstract

    Numerous inflammatory cytokines have been implicated in the pathogenesis of cardiovascular diseases. Monocyte chemoattractant protein (MCP)-1/CCL2 is expressed by mainly inflammatory cells and stromal cells such as endothelial cells, and its expression is upregulated after proinflammatory stimuli and tissue injury. MCP-1 can function as a traditional chemotactic cytokine and also regulates gene transcription. The recently discovered novel zinc-finger protein, called MCPIP (MCP-1-induced protein), initiates a series of signaling events that causes oxidative and endoplasmic reticulum (ER) stress, leading to autophagy that can result in cell death or differentiation, depending on the cellular context. After a brief review of the basic processes involved in inflammation, ER stress, and autophagy, the recently elucidated role of MCP-1 and MCPIP in inflammatory diseases is reviewed. MCPIP was found to be able to control inflammatory response by inhibition of nuclear factor-kappa B activation through its deubiquitinase activity or by degradation of mRNA encoding a set of inflammatory cytokines through its RNase activity. The potential inclusion of such a novel deubiquitinase in the emerging anti-inflammatory strategies for the treatment of inflammation-related diseases such as cardiovascular diseases and type 2 diabetes is briefly discussed. (Circ Res. 2012;110:174-189.)

    Journal Title

    Circulation Research

    Volume

    110

    Issue/Number

    1

    Publication Date

    1-1-2012

    Document Type

    Review

    Language

    English

    First Page

    174

    Last Page

    189

    WOS Identifier

    WOS:000299023800020

    ISSN

    0009-7330

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