CCL2/Monocyte Chemoattractant Protein-1 Regulates Inflammatory Responses Critical to Healing Myocardial Infarcts

By O. Dewald, P. Zymek, K. Winkelmann, Anna Koerting, G. Ren, Tareq Abou-Khamis, L. Michael, B. Rollins, M. Entman, Nikolaos G. Frangogiannis. Circulation Research, 2005

728 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/a06e2b45f39cd116c2674cd03c3f1fc3bc08e4cf

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cardiology and Cardiovascular Medicine

In Molecular Biology

In Oncology

Nikolaos G. Frangogiannis

Citations in the corpus

Cardiac fibrosis. (2020, background): “of monocytes and macrophages expressing the main CCL2 receptor, CCR2, resulting in up-regulation of fibrogenic mediators, such as TGF-b and osteopontin.(128,129,137) Although CCL2 has been suggested to pro-”
Paracrine Factors of Mesenchymal Stem Cells Recruit Macrophages and Endothelial Lineage Cells and Enhance Wound Healing (2008, background): “MIP and MCP are major chemoattractants for monocytes/macrophages and play a key role in macrophage infiltration during wound healing [33,34].”
The Pathogenesis of Cardiac Fibrosis (2013, neutral): “During the early inflammatory phase of infarct healing [2], monocytes with pro-inflammatory, phagocytic, and proteolytic properties are recruited; these cells express the chemokine receptor CCR2 and infiltrate the infarcted myocardium in response to the marked upregulation of the CC chemokine monocy”
Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities (2018, background): “Genetic ablation of MCP-1 or its receptor, chemokine receptor 2 (CCR2), reduced recruitment of proinflammatory monocytes, and decreased cytokine expression in the infarct zone, and prevented adverse remodeling following AMI (Dewald et al., 2005).”
Pathophysiology of Myocardial Infarction (2015, neutral): “During the first few hours after reperfusion, complement activation, induction of the CC chemokine CCL2 and activation of TGF-β play an important role in recruitment of proinflammatory monocytes in the infarcted myocardium (24,82,268).”
The role of TGF-β Signaling in Myocardial Infarction and Cardiac Remodeling (2007, background): “Complement activation, free radical generation and monocyte chemoattractant chemokines also play a crucial role in recruiting mononuclear cells in the infarcted myocardium [47, 54 ].”
The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. (2016, background): “Early recruitment of proinflammatory Ly6C monocytes is mediated through the activation of the MCP-1/CCR2 axis.(117) At a later stage, anti-inflammatory monocyte subpopulations are selectively recruited and may participate in resolution of the postinfarction inflammatory response.”