Key result
Murine models of cardiometabolic HFpEF highlight mechanisms of inflammation, oxidative stress, and endothelial dysfunction.
Why the study?
Heart failure with preserved ejection fraction accounts for most heart failure cases worldwide, but therapeutic strategies remain inadequate.
Understanding murine models of cardiometabolic HFpEF provides insight into disease mechanisms and can aid in the development of effective therapeutic interventions.
May inform preclinical HFpEF therapy development; leaves open human translation.
Heart failure with preserved ejection fraction (HFpEF) remains a significant challenge in modern healthcare. It accounts for the majority of heart failure cases and their number worldwide is steadily increasing. With its high prevalence and substantial clinical impact, therapeutic strategies for HFpEF are still inadequate. This review focuses on the cardiometabolic phenotype of HFpEF which is characterised by such conditions as obesity, type 2 diabetes mellitus, and hypertension. Various murine models that mimic this phenotype are discussed. Each model's pathophysiological aspects, namely inflammation, oxidative stress, endothelial dysfunction, changes in cardiomyocyte protein function, and myocardial metabolism alterations are examined in detail. Understanding these models can provide insight into the mechanisms underlying HFpEF and aid in the development of effective therapeutic interventions.
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Ogurtsova et al. (2025) conducted a review in Heart failure with preserved ejection fraction (HFpEF). Murine models was evaluated. Murine models mimicking the cardiometabolic phenotype of HFpEF provide insights into pathophysiological mechanisms such as inflammation, oxidative stress, and endothelial dysfunction.
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