Recent Updates on the Role of Genetic and Epigenetic Factors in the Pathogenesis of the Metabolic Syndrome.

BACKGROUND

Metabolic syndrome (MetS) is a multifactorial disorder characterized by obesity, hypertension, dyslipidemia, and diabetes, all of which contribute to the global burden of cardiovascular diseases. Growing evidence highlights the interplay between genetic predisposition and epigenetic modifications in shaping susceptibility to MetS and its complications.

SCOPE OF REVIEW: This systematic review analyzed 55 relevant studies published in the last decade, exploring genetic polymorphisms, DNA methylation, and non-coding RNAs (ncRNAs) associated with MetS.

RESULT AND

CONCLUSION

Our findings reveal that MetS arises from the convergence of inherited genomic risk and environmentally driven epigenetic reprogramming in the forms of DNA methylation changes and ncRNAs involvement, which affect important genes related to crucial biological functions such as neuroendocrine, adipogenesis and insulin signaling, glucose and lipid metabolism, and immune response and inflammatory signaling. Understanding these interactions may facilitate the development of predictive biomarkers and targeted interventions to mitigate cardiometabolic risks.