Metabolic syndrome (MS) is a chronic non‐infective syndrome characterised clinically by a set of vascular risk factors that include insulin resistance, hypertension, abdominal obesity, impaired glucose metabolism, and dyslipidaemia. These risk factors are due to a pro‐inflammatory state, oxidative stress, haemodynamic dysfunction, and ischaemia, which overlap in ‘dysmetabolic’ patients. This review aimed to evaluate the relationship between the traditional components of MS with cardiovascular disease (CVD), inflammation, and oxidative stress. MEDLINE‐PubMed, EMBASE, and Cochrane databases were searched. Chronic low‐grade inflammatory states and metaflammation are often accompanied by metabolic changes directly related to CVD incidence, such as diabetes mellitus, hypertension, and obesity. Moreover, the metaflammation is characterised by an increase in the serum concentration of pro‐inflammatory cytokines, mainly interleukin‐1 β (IL‐1β), IL‐6, and tumour necrosis factor‐α (TNF‐α), originating from the chronically inflamed adipose tissue and associated with oxidative stress. The increase of reactive oxygen species overloads the antioxidant systems causing post‐translational alterations of proteins, lipids, and DNA leading to oxidative stress. Hyperglycaemia contributes to the increase in oxidative stress and the production of advanced glycosylation end products (AGEs) which are related to cellular and molecular dysfunction. Oxidative stress and inflammation are associated with cellular senescence and CVD. CVD should not be seen only as being triggered by classical MS risk factors. Atherosclerosis is a multifactorial pathological process with several triggering and aetiopathogenic mechanisms. Its medium and long‐term repercussions, however, invariably constitute a significant cause of morbidity and mortality. Implementing preventive and therapeutic measures against oxy‐reductive imbalances and metaflammation states has unquestionable potential for favourable clinical outcomes in cardiovascular medicine.

Adipose, skeletal, and hepatic muscle tissues are the main endocrine organs that produce adipokines, myokines, and hepatokines. These biomarkers can be harmful or beneficial to an organism and still perform crosstalk, acting through the endocrine, paracrine, and autocrine pathways. This study aims to review the crosstalk between adipokines, myokines, and hepatokines. Far beyond understanding the actions of each biomarker alone, it is important to underline that these cytokines act together in the body, resulting in a complex network of actions in different tissues, which may have beneficial or non-beneficial effects on the genesis of various physiological disorders and their respective outcomes, such as type 2 diabetes mellitus (DM2), obesity, metabolic syndrome, and cardiovascular diseases (CVD). Overweight individuals secrete more pro-inflammatory adipokines than those of a healthy weight, leading to an impaired immune response and greater susceptibility to inflammatory and infectious diseases. Myostatin is elevated in pro-inflammatory environments, sharing space with pro-inflammatory organokines, such as tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), resistin, and chemerin. Fibroblast growth factor FGF21 acts as a beta-oxidation regulator and decreases lipogenesis in the liver. The crosstalk mentioned above can interfere with homeostatic disorders and can play a role as a potential therapeutic target that can assist in the methods of diagnosing metabolic syndrome and CVD.

Skeletal muscle is capable of secreting different factors in order to communicate with other tissues. These mediators, the myokines, show potentially far-reaching effects on non-muscle tissues and can provide a molecular interaction between muscle and body physiology. Sarcopenia is a chronic degenerative neuromuscular disease closely related to cardiomyopathy and chronic heart failure, which influences the production and release of myokines. Our objective was to explore the relationship between myokines, sarcopenia, and cardiovascular diseases (CVD). The autocrine, paracrine, and endocrine actions of myokines include regulation of energy expenditure, insulin sensitivity, lipolysis, free fatty acid oxidation, adipocyte browning, glycogenolysis, glycogenesis, and general metabolism. A sedentary lifestyle accelerates the aging process and is a risk factor for developing sarcopenia, metabolic syndrome, and CVD. Increased adipose tissue resulting from the decrease in muscle mass in patients with sarcopenia may also be involved in the pathology of CVD. Myokines are protagonists in the complex condition of sarcopenia, which is associated with adverse clinical outcomes in patients with CVD. The discovery of new pathways and the link between myokines and CVD remain a cornerstone toward multifaceted interventions and perhaps the minimization of the damage resulting from muscle loss induced by factors such as atherosclerosis.