Adipose tissue inflammation and metabolic dysfunction in obesity.
adipocytes
immunity
inflammation
insulin resistance
obesity
Journal
American journal of physiology. Cell physiology
ISSN: 1522-1563
Titre abrégé: Am J Physiol Cell Physiol
Pays: United States
ID NLM: 100901225
Informations de publication
Date de publication:
01 03 2021
01 03 2021
Historique:
pubmed:
29
12
2020
medline:
31
3
2021
entrez:
28
12
2020
Statut:
ppublish
Résumé
Several lines of preclinical and clinical research have confirmed that chronic low-grade inflammation of adipose tissue is mechanistically linked to metabolic disease and organ tissue complications in the overweight and obese organism. Despite this widely confirmed paradigm, numerous open questions and knowledge gaps remain to be investigated. This is mainly due to the intricately intertwined cross-talk of various pro- and anti-inflammatory signaling cascades involved in the immune response of expanding adipose depots, particularly the visceral adipose tissue. Adipose tissue inflammation is initiated and sustained over time by dysfunctional adipocytes that secrete inflammatory adipokines and by infiltration of bone marrow-derived immune cells that signal via production of cytokines and chemokines. Despite its low-grade nature, adipose tissue inflammation negatively impacts remote organ function, a phenomenon that is considered causative of the complications of obesity. The aim of this review is to broadly present an overview of adipose tissue inflammation by highlighting the most recent reports in the scientific literature and summarizing our overall understanding of the field. We also discuss key endogenous anti-inflammatory mediators and analyze their mechanistic role(s) in the pathogenesis and treatment of adipose tissue inflammation. In doing so, we hope to stimulate studies to uncover novel physiological, cellular, and molecular targets for the treatment of obesity.
Identifiants
pubmed: 33356944
doi: 10.1152/ajpcell.00379.2020
pmc: PMC8294624
doi:
Substances chimiques
Cytokines
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
C375-C391Subventions
Organisme : HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
ID : DK096521
Organisme : NIDDK NIH HHS
ID : R01 DK096521
Pays : United States
Organisme : HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)
ID : HL117724
Organisme : NHLBI NIH HHS
ID : R01 HL117724
Pays : United States
Organisme : HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)
ID : HL141108
Organisme : NHLBI NIH HHS
ID : R01 HL141108
Pays : United States
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