Adipokines: a link between obesity and cardiovascular disease

Abstract

Obesity is a risk factor for various cardiovascular diseases including hypertension, atherosclerosis, and myocardial infarction. Recent studies aimed at understanding the microenvironment of adipose tissue and its impact on systemic metabolism have shed light on the pathogenesis of obesity-linked cardiovascular diseases. Adipose tissue functions as an endocrine organ by secreting multiple immune-modulatory proteins known as adipokines. Obesity leads to increased expression of pro-inflammatory adipokines and diminished expression of anti-inflammatory adipokines, resulting in the development of a chronic, low-grade inflammatory state. This adipokine imbalance is thought to be a key event in promoting both systemic metabolic dysfunction and cardiovascular disease. This review will focus on the adipose tissue microenvironment and the role of adipokines in modulating systemic inflammatory responses that contribute to cardiovascular disease.

Keywords: Adiponectin; Cardiovascular disease; Leptin; Sfrp5; TNFα.

Figure 1. Obesity-linked changes in adipose tissue composition

Obesity can promote changes in adipose tissue and promote the transition to a metabolically dysfunctional phenotype. As the body develops obesity, adipocytes undergo hypertrophy due to the increased storage of triglycerides. Macrophages in lean fat express markers of a M2 or “alternatively activated” state, whereas obesity leads to recruitment and accumulation of a M1 or “classically activated” state with macrophages and CD8⁺ T cells in adipose tissue. Metabolically dysfunctional adipose tissue is indicated by the presence of crown-like histological structures that represent activated M1-like macrophages surrounding a necrotic adipocyte and CD4⁺ T cells. Anti-inflammatory adipokines, such as adiponectin are preferentially produced by lean adipose tissue, whereas high levels of pro-inflammatory factors are produced in obese states.