Роль телоцитов в ремоделировании миокарда и развитии сердечно-сосудистых осложнений у пациентов с хронической сердечной недостаточностью после коронарного шунтирования Ключевые слова: телоциты, ремоделирование миокарда, сердечная недостаточность, коронарное шунтирование, осложнения

Osteoarthritis associated with metabolic syndrome (MetOA) is a clinical phenotype defined by the role of obesity and metabolic syndrome as risk factors, as well as mild chronic inflammation. Obesity is an established risk factor for developing osteoarthritis (OA) not only in the knee but also in the hands. Metabolic syndrome is also a risk factor for the development of OA, and the cumulative effect of the various components of the syndrome is combined with the independent action of each individual component (diabetes mellitus, dyslipidemia and/or arterial hypertension). The higher incidence of OA in obese patients is associated with several factors. One of them is a large fat mass, which increases the stress on the joints. Another is the production of pro-inflammatory mediators by adipose tissue, which negatively affect the tissues of the joints. Finally, patients with OA, with or without metabolic syndrome, are at increased risk of cardiovascular mortality, not only due to a sedentary lifestyle, but also due to common risk factors. Among them is the mild inflammation seen in patients with metabolic disorders. Thus, primary prevention and appropriate treatment of obesity and metabolic syndrome can delay the development and slow the progression of OA.

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This study was done in order to establish an expression pattern of the melatonin MT2 receptors (MT2R) in LV cardiac myocytes (CM) of female rats with hypoestrogenism and heart failure. Hypoestrogenism (hypo‐E) was induced by bilateral ovariectomy and heart failure (HF) was caused by s.c. injection of a 1% mezaton solution (0.1ml) followed by an intensive swimming regimen for 14 days. Thirty adult outbred female rats were used: 10 rats with a combination of hypo‐E and HF (hypo‐E/HF); 10 rats with HF only; 5 rats with hypo‐E only; and 5 intact rats served as a control. At the end of experiment, the MT2R immunoreactivity (MT2R‐IR) was detected by immunohistochemistry with an anti‐MTNR1B antibody. The localization and intensity of MT2R‐IR were assessed in a double‐blind manner on a semiquantitative rating scale using the following criteria: (‐) no MT2R‐IR; (+) slight MT2R‐IR, a few immunopositive CM; (++) moderate MT2R‐IR, more than 5 immunopositive CM on each section; (+++) high MT2R‐IR, almost all CM are immunopositive. We found that in control rats the CM showed a slight to moderate level of MT2R‐IR (+/++), while in HF the CM revealed the highest level of MT2R‐IR (+++). The reduced MT2R‐IR was observed in rats with hypo‐E only (+), whereas the animals from the hypo‐E/HF group showed the lowest level of MT2R‐IR (‐/+). Our findings demonstrate that chronic hypoestrogenism inhibits a cardioprotective increase in MT2R induced by HF.