The Epigenetic Role of MiRNAs in Endocrine Crosstalk Between the Cardiovascular System and Adipose Tissue: A Bidirectional View

Abstract

Overweight and obesity (OBT) is a serious health condition worldwide, and one of the major risk factors for cardiovascular disease (CVD), the main reason for morbidity and mortality worldwide. OBT is the proportional increase of Adipose Tissue (AT) compared with other tissue and fluids, associated with pathological changes in metabolism, hemodynamic overload, cytokine secretion, systemic inflammatory profile, and cardiac metabolism. In turn, AT is heterogeneous in location, and displays secretory capacity, lipolytic activation, insulin sensitivity, and metabolic status, performing anatomic, metabolic, and endocrine functions. Evidence has emerged on the bidirectional crosstalk exerted by miRNAs as regulators between the heart and AT on metabolism and health conditions. Here, we discuss the bidirectional endocrine role of miRNAs between heart and AT, rescuing extracellular vesicles’ (EVs) role in cell-to-cell communication, and the most recent results that show the potential of common therapeutic targets through the elucidation of parallel and ⁄or common epigenetic mechanisms.

Role of Human Epicardial Adipose Tissue–Derived miR-92a-3p in Myocardial Redox State

“…Adipose tissue communicates with the cardiovascular system via the secretion of endocrine and paracrine signals, which include adipokines/adipocytokines, 3 , 24 lipid species, 25 microRNAs, 26 and other molecules. 12 Although, under physiological conditions, adipose tissue supports cardiovascular health, its secretome in the presence of metabolic dysregulation becomes detrimental to the cardiovascular system.…”

The Role of Epicardial Adipose Tissue-Derived MicroRNAs in the Regulation of Cardiovascular Disease: A Narrative Review

“…To date, a number of studies have examined the expression of EAT-derived miRNAs in relation to CVDs [ 85 , 86 , 87 , 88 , 89 , 90 , 91 ]. However, it is practically impossible to review all the EAT-derived miRNAs differentially expressed during the course of CVDs because a sizable portion of them have not been empirically examined pertaining to their possible impact on the cardiovascular system.…”

Early growth response-1: Key mediators of cell death and novel targets for cardiovascular disease therapy

“…Egr-1 knockdown converts pathological hypertrophy to physiological hypertrophy by activating the AKT pathway. The miR-99 family regulates Akt/mTOR/IGF1 (Insulin Like Growth Factor 1) via Egr-1 -mediated expression, which governs both pathological and healthy hypertrophy ( 103 ). AKT1 silencing reduces EGR1 phosphorylation, which decreases miR-99 transcription, resulting in lower apoptosis and cytotoxicity levels.…”