The Sick Adipose Tissue: New Insights Into Defective Signaling and Crosstalk With the Myocardium

Abstract

Adipose tissue (AT) biology is linked to cardiovascular health since obesity is associated with cardiovascular disease (CVD) and positively correlated with excessive visceral fat accumulation. AT signaling to myocardial cells through soluble factors known as adipokines, cardiokines, branched-chain amino acids and small molecules like microRNAs, undoubtedly influence myocardial cells and AT function via the endocrine-paracrine mechanisms of action. Unfortunately, abnormal total and visceral adiposity can alter this harmonious signaling network, resulting in tissue hypoxia and monocyte/macrophage adipose infiltration occurring alongside expanded intra-abdominal and epicardial fat depots seen in the human obese phenotype. These processes promote an abnormal adipocyte proteomic reprogramming, whereby these cells become a source of abnormal signals, affecting vascular and myocardial tissues, leading to meta-inflammation, atrial fibrillation, coronary artery disease, heart hypertrophy, heart failure and myocardial infarction. This review first discusses the pathophysiology and consequences of adipose tissue expansion, particularly their association with meta-inflammation and microbiota dysbiosis. We also explore the precise mechanisms involved in metabolic reprogramming in AT that represent plausible causative factors for CVD. Finally, we clarify how lifestyle changes could promote improvement in myocardiocyte function in the context of changes in AT proteomics and a better gut microbiome profile to develop effective, non-pharmacologic approaches to CVD.

Exploring the Links between Obesity and Psoriasis: A Comprehensive Review

“…Nevertheless, as obesity progresses, preadipocyte differentiation becomes dysfunctional, leading to reduced insulin signalling, glucose uptake and adiponectin release by mature adipocytes. This process is due to at least two phenomena: Firstly, the growth and expansion of adipose tissue due to hypertrophy restrict oxygen diffusion from the capillaries to the adipocytes, producing hypoxia [ 84 ]. The second, palmitic acid from the high-fat diet or lipolysis, drives endoplasmic reticulum (ER) stress and unfolded protein response (UPR) activation [ 85 , 86 ].…”

Restricted T-Cell Repertoire in the Epicardial Adipose Tissue of Non-ST Segment Elevation Myocardial Infarction Patients

“…However, the functional role of the adipose tissue surrounding the heart is still barely elucidated. Several clues indicate that EAT is one of the key characteristics of CAD pathophysiology (25)(26)(27). Therefore, in addition to its storage and protective functions, EAT must be considered by all accounts a lymphatic organ, characterized by leukocyte trafficking and cytokine and adipokine release.…”

Metabolic Changes in Obesity

“…They are considered specialized cells that store lipids, but this is not their primary purpose, as evidenced by beta cells, muscle cells, and neurons [14]. Mature adipocytes develop when markers include the expression and adipocyte-associated hormones, cytokines, and enzymes associated with lipid storage and release into the bloodstream [14].…”

“…Perhaps the most interesting aspect of adipocyte differentiation is the way in which preadipocytes are added to the adipocyte repertoire, a repertoire of peroxisome-activated receptor family members and protein receptors that bind CCAAT enhancers [14].…”