| Autor: |
Sokolova M; Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.; Department of Immunology, Oslo University Hospital Rikshospitalet and University of Oslo, Oslo, Norway., Ranheim T; Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.; Institute of Clinical Medicine, The Faculty of Medicine, University of Oslo, Oslo, Norway., Louwe MC; Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.; Department of Immunology, Oslo University Hospital Rikshospitalet and University of Oslo, Oslo, Norway., Halvorsen B; Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.; Institute of Clinical Medicine, The Faculty of Medicine, University of Oslo, Oslo, Norway., Yndestad A; Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway., Aukrust P; Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.; Department of Immunology, Oslo University Hospital Rikshospitalet and University of Oslo, Oslo, Norway.; Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital Rikshospitalet, Oslo, Norway. |
| Abstrakt: |
Metabolic and immune systems are among the most fundamental requirements for survival. Many metabolic and immune response pathways or nutrient- and pathogen-sensing systems are evolutionarily conserved throughout species. As a result, the immune response and metabolic regulation are highly integrated and the proper function of each is dependent on the other. This interaction between metabolic disturbances and the immune system has been most extensively studied in disorders related to obesity such as insulin resistance, type 2 diabetes, and nonalcoholic fatty liver disease. Metabolically induced inflammation seems also to play a role in the development and progression of atherosclerosis including its complications such as myocardial infarction (MI) and post-MI remodeling. There are several lines of evidence suggesting that NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is a sensor of metabolic stress linking metabolic disturbances to inflammation. Here, we will discuss the role of the NLRP3 inflammasome in the pathogenesis of obesity and diabetes, 2 important risk factors for atherosclerosis and MI. We will also discuss the role of NLRP3 inflammasome in the interaction between metabolic disturbances and myocardial inflammation during MI and during metabolically induced myocardial remodeling. |
