Is obesity-induced ECM remodeling a prelude to the development of various diseases?

Azam Rahimi, Mehdi Rasouli, Saeed Heidari keshel, Maryam Ebrahimi, Farzad Pakdel

Research output: Contribution to journalReview articlepeer-review

2 Scopus citations

Abstract

Due to the increasing incidence rate of obesity worldwide and the associated complications such as type 2 diabetes and cardiovascular diseases, research on the adipose tissue physiology and the role of the extracellular matrix (ECM) has gained tremendous attention. The ECM, one of the most crucial components in body tissues, undergoes remodeling and regeneration of its constituents to guarantee normal tissue function. There is a crosstalk between fat tissue and various body organs, including but not limited to the liver, heart, kidney, skeletal muscle, and so forth. These organs respond to fat tissue signals through changes in ECM, function, and their secretory products. Obesity can cause ECM remodeling, inflammation, fibrosis, insulin resistance, and disrupted metabolism in different organs. However, the mechanisms underlying the reciprocal communication between various organs during obesity are still not fully elucidated. Gaining a profound knowledge of ECM alterations during the progression of obesity will pave the way toward developing potential strategies to either circumvent pathological conditions or open an avenue to treat complications associated with obesity.

Original languageEnglish (US)
Pages (from-to)95-101
Number of pages7
JournalObesity Research and Clinical Practice
Volume17
Issue number2
DOIs
StatePublished - Mar 1 2023
Externally publishedYes

Keywords

  • Extracellular matrix
  • Insulin resistance
  • Obesity
  • Organ crosstalk
  • Organ dysfunction
  • Remodeling

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Nutrition and Dietetics

Fingerprint

Dive into the research topics of 'Is obesity-induced ECM remodeling a prelude to the development of various diseases?'. Together they form a unique fingerprint.

Cite this