Does C-C Motif Chemokine Ligand 2 (CCL2) Link Obesity to a Pro-Inflammatory State?

Int J Mol Sci. 2021 Feb 2;22(3):1500. doi: 10.3390/ijms22031500.

Abstract

The mechanisms of how obesity contributes to the development of cardio-metabolic diseases are not entirely understood. Obesity is frequently associated with adipose tissue dysfunction, characterized by, e.g., adipocyte hypertrophy, ectopic fat accumulation, immune cell infiltration, and the altered secretion of adipokines. Factors secreted from adipose tissue may induce and/or maintain a local and systemic low-grade activation of the innate immune system. Attraction of macrophages into adipose tissue and altered crosstalk between macrophages, adipocytes, and other cells of adipose tissue are symptoms of metabolic inflammation. Among several secreted factors attracting immune cells to adipose tissue, chemotactic C-C motif chemokine ligand 2 (CCL2) (also described as monocyte chemoattractant protein-1 (MCP-1)) has been shown to play a crucial role in adipose tissue macrophage infiltration. In this review, we aimed to summarize and discuss the current knowledge on CCL2 with a focus on its role in linking obesity to cardio-metabolic diseases.

Keywords: adipokine; adipose tissue; chemokine; inflammation; obesity.

Publication types

  • Review

MeSH terms

  • Adipocytes / physiology
  • Adipose Tissue / metabolism
  • Animals
  • Autoimmune Diseases / genetics
  • Autoimmune Diseases / metabolism
  • Cardiovascular Diseases / genetics
  • Cardiovascular Diseases / metabolism
  • Chemokine CCL2 / deficiency
  • Chemokine CCL2 / genetics
  • Chemokine CCL2 / physiology*
  • Chemokines / metabolism
  • Humans
  • Inflammation / complications*
  • Inflammation / genetics
  • Inflammation / physiopathology
  • Insulin Resistance
  • Macrophages / physiology
  • Mesenchymal Stem Cells / metabolism
  • Metabolic Syndrome / genetics
  • Metabolic Syndrome / metabolism
  • Mice
  • Mice, Knockout
  • Models, Animal
  • Molecular Targeted Therapy
  • Neoplasm Proteins / metabolism
  • Neoplasms / metabolism
  • Neoplasms / pathology
  • Neural Tube Defects / genetics
  • Neural Tube Defects / metabolism
  • Obesity / etiology*
  • Obesity / genetics
  • Obesity / physiopathology
  • Polymorphism, Single Nucleotide
  • Signal Transduction

Substances

  • CCL2 protein, human
  • Ccl2 protein, mouse
  • Chemokine CCL2
  • Chemokines
  • Neoplasm Proteins