Key result
Bariatric surgery normalizes obesity-induced LV dysfunction and reduces myocardial fibrosis and infarct size in rodents.
Why the study?
Although bariatric surgery shows positive clinical effects on cardiovascular diseases, data on the underlying physiological and molecular biological mechanisms remain relatively scarce.
Does bariatric surgery improve cardiovascular pathology in experimental animal models?
Systematic Review
Does bariatric surgery improve cardiovascular pathology in experimental animal models?
Answers are grounded in this paper and cite their sources.
This systematic review of experimental rodent models demonstrates that bariatric surgery improves cardiovascular pathology through mechanisms including AMPK activation, increased nitric oxide, and elevated GLP-1.
Obesity and pathogenetically related cardiovascular diseases (CVDs) are among the most significant public health challenges worldwide. By exerting a combined negative impact on health, they substantially increase disability and mortality rates of the global population. Bariatric surgery is currently the most effective treatment for obesity, and the results of numerous clinical trials demonstrate its positive effects on the course of such CVDs as arterial hypertension, coronary artery disease, atrial fibrillation, and chronic heart failure. However, data on the physiological and molecular biological basics of these effects remain relatively scarce. The mechanisms underlying the beneficial influence of bariatric interventions on CVDs can be divided into those dependent on and those independent of body weight loss. Experimental studies in animals, conducted under controlled laboratory conditions, enable the identification of the major pathways responsible for the compensation of CVDs following gastrointestinal surgical interventions in obesity. In this systematic review, we analyze the available experimental studies investigating the impact of bariatric surgery on the manifestations of cardiovascular pathology using appropriate models, including arterial hypertension, diabetic cardiomyopathy, myocardial ischemia–reperfusion injury, and obesity‑induced myocardial dysfunction. It is shown that nearly all research in this area has been performed in rodents. Bariatric procedures, particularly gastric bypass and sleeve gastrectomy, are accompanied by the normalization of obesity‑induced left ventricular systolic and diastolic dysfunction, reduction of myocardial fibrosis in diabetic cardiomyopathy, reduction of infarct size following myocardial ischemia–reperfusion injury, and a decrease in the incidence and severity of arterial hypertension. The implicated molecular mechanisms include the activation of AMP‑activated protein kinase, increased production and bioavailability of nitric oxide, and elevated stimulated secretion levels of glucagon‑like peptide‑1. It is evident that the molecular mechanisms of the beneficial cardiovascular effects of bariatric surgery warrant further investigation.
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Kravchuk et al. (2026) conducted a systematic review in Obesity and cardiovascular diseases. Bariatric surgery was evaluated on Manifestations of cardiovascular pathology. Bariatric surgery in experimental rodent models normalized obesity-induced left ventricular dysfunction, reduced myocardial fibrosis and infarct size, and decreased arterial hypertension severity.
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