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Adipose Tissue Fibrosis in Obesity: Etiology and Challenges

期刊

ANNUAL REVIEW OF PHYSIOLOGY
卷 84, 期 -, 页码 135-155

出版社

ANNUAL REVIEWS
DOI: 10.1146/annurev-physiol-060721-092930

关键词

obesity; adipose tissue; fibrosis; progenitors; adipogenesis; macrophages

资金

  1. Fondation pour la Recherche Medicale
  2. French National Agency of Research
  3. research program CAPES-COFECUB (Coordination pour le Perfectionnement du Personnel de l'Enseignement Superieur-Comite Francais d'Evaluation de la Cooperation Universitaire et Scientifique avec le Bresil)
  4. European Foundation for the Study of Diabetes
  5. Societe Francaise de Nutrition
  6. Association Francaise d'Etude et de Recherche sur l'Obesite
  7. L'Institut Benjamin Delessert
  8. RHU-CARMMA (Reseau Hospitalo-Universitaire-Cardiac and Skeletal Muscle Alteration in Relation to Metabolic Diseases and Aging) grant from the National Agency of Research [ANR-15-RHUS-0003]

向作者/读者索取更多资源

Obesity is a chronic and progressive condition that affects whole-body energy balance and is linked to the development of comorbidities. Fibrotic adipose tissue caused by obesity can lead to metabolic dysfunctions such as insulin resistance. Targeting inflammation or fibrosis deposition may help improve insulin resistance and glucose homeostasis in individuals with obesity.
Obesity is a chronic and progressive process affecting whole-body energy balance and is associated with comorbidity development. In addition to increased fat mass, obesity induces white adipose tissue (WAT) inflammation and fibrosis, leading to local and systemic metabolic dysfunctions, such as insulin resistance (IR). Accordingly, limiting inflammation or fibrosis deposition may improve IR and glucose homeostasis. Although no targeted therapy yet exists to slow or reverse adipose tissue fibrosis, a number of findings have clarified the underlying cellular and molecular mechanisms. In this review, we highlight adipose tissue remodeling events shown to be associated with fibrosis deposition, with a focus on adipose progenitors involved in obesity-induced healthy as well as unhealthy WAT expansion.

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