Obesity-Induced Changes in Adipose Tissue Microenvironment and Their Impact on Cardiovascular Disease

Abstract

Obesity is causally linked with the development of cardiovascular disorders. Accumulating evidence indicates that cardiovascular disease is the “collateral damage” of obesity-driven adipose tissue dysfunction that promotes a chronic inflammatory state within the organism. Adipose tissues secrete bioactive substances, referred to as adipokines, which largely function as modulators of inflammation. The microenvironment of adipose tissue will affect the adipokine secretome, having actions on remote tissues. Obesity typically leads to the upregulation of pro-inflammatory adipokines and the downregulation of anti-inflammatory adipokines, thereby contributing to the pathogenesis of cardiovascular diseases. In this review, we focus on the microenvironment of adipose tissue and how it influences cardiovascular disorders, including atherosclerosis and ischemic heart diseases, through the systemic actions of adipokines.

ANGPTL2 ― A New Causal Player in Accelerating Heart Disease Development in the Aging ―

“…In terms of the mechanisms linking these conditions, accumulating evidence suggests that inflammatory changes in perivascular fat, which is distributed ubiquitously around arteries throughout the body, may have a direct role in promoting the pathogenesis of vascular diseases accelerated by obesity. 43- 45 Interestingly, in obesity, chronic inflammation occurs in both visceral and perivascular adipose tissues. 44, 45 In obese mice, the expression of ANGPTL2 is increased in perivascular adipose tissues surrounding the femoral artery at levels equivalent to those seen in visceral adipose tissues.…”

“…43- 45 Interestingly, in obesity, chronic inflammation occurs in both visceral and perivascular adipose tissues. 44, 45 In obese mice, the expression of ANGPTL2 is increased in perivascular adipose tissues surrounding the femoral artery at levels equivalent to those seen in visceral adipose tissues. 46 In mice, we have undertaken adipose tissue transplantation experiments that show that adipose tissue-secreted ANGPTL2 accelerates vascular inflammation, pathologic vascular tissue remodeling and subsequent CVD development.…”

Perivascular adipose tissue and coronary atherosclerosis

“…This phenomenon, often described as ‘obesity paradox’, highlights the complex biology of adipose tissue (AT) and its variable effects on the cardiovascular system. BMI, despite its widespread use, fails to take into account variations in AT quality and distribution, which are now established as key determinants of its cardiometabolic effects 3. Depot-specific differences in the ability of AT to store lipids as well as its secretome profile are important in understanding the complex association of AT with cardiovascular disease 2…”

“…This may eventually progress to adipocyte dysfunction and apoptosis, with subsequent inflammatory cell infiltration, late capillary rarefaction and, ultimately, fibrosis 14. This AT remodelling generates a systemic chronic, low-grade inflammatory state as a result of a shift in the adipocyte phenotype from a protective profile to an imbalanced production of proinflammatory, pro-oxidant and profibrotic adipokines, such as leptin, resistin and visfatin 3. Of note, these biological variations are depot specific.…”

CD4+ T lymphocytes produce adiponectin in response to transplants

“…Numerous studies have correlated low levels of adiponectin in the circulation with vascular inflammation (10). However, the significance of this correlation varies greatly among studies.…”