Table 1.

The comparison between the risk factors and associated molecular pathways involved in the development of diabetes (DM) and cardiovascular disease (CVD).

Risk Factors	Diabetes	CVD
Inflammatory factors	increased insulin resistance by IRS-1 [70]	endothelial injury, dysregulation of coagulation [71]
Oxidative stress	increased hexosamine pathway of glucose oxidation [72]	impaired mitochondrial electron transport, damage of DNA, leading to activation of stress-sensitive pathways [73]
Epigenetics	methylation of INS, PDX1, PPARGC1A, and GLP1R [74]	hydroxymethylation of myosin heavy chain 7, inhibition of BET protein [75]
Lipid dysregulations	higher amount of VLDL [76]	increased risk of atherosclerosis [62,76]
Sleep apnoea	apnoea resulting in lower tissue sensitivity to insulin [63,64,65]	multifactorial pathophysiological processes resulting in HTN [77]
NAFLD	leading to bigger insulin resistance [68,69]	increased risk of myocardial infarction and brain stroke [78]
PCOS	higher risk of insulin resistance [76,77]	higher risk of hypertension in post-reproductive life [79]
RAAS	higher NADPH activity, resulting in cardiac dysfunction [80,81]	leading to local inflammation, which causes arterial thrombosis [82]
mRNA	m6A mRNA methylation [83]	m6A mRNA methylation [84]

NAFLD—non-alcoholic fatty liver disease; PCOS—polycystic ovary syndrome; RAAS—renin–angiotensin–aldosterone system; mRNA—messenger ribonucleic acid; IRS-1—insulin receptor substrate-1; DNA—deoxyribonucleic acid; INS—insulin gene; PDX1—pancreatic and duodenal homeobox 1 gene; PPARGC1A—peroxisome-proliferator-activated receptor gamma coactivator 1-alpha gene; GLP1R—glucagon-like peptide-1 receptor gene; BET—bromodomain and extra-terminal domain; HTN—hypertension; VLDL—very-low-density lipoprotein; NADPH—nicotinamide adenine dinucleotide phosphate.