Cardiovascular diseases (CVD) are closely linked to protein homeostasis (proteostasis) and its failure. Beside genetic mutations that impair cardiac protein quality control, obesity is a strong risk factor for heart disease. In obesity, adipose tissue becomes dysfunctional and impacts heart function and CVD progression by releasing cytokines that contribute to systemic insulin resistance and cardiovascular dysfunction. In addition, chronic inflammation and lipotoxicity compromise endoplasmic reticulum (ER) function, eliciting stress responses that overwhelm protein quality control beyond its capacity. Impairment of proteostasis—including dysfunction of the ubiquitin–proteasome system (UPS), autophagy, and the depletion of chaperones—is intricately linked to cardiomyocyte dysfunction. Interventions targeting UPS and autophagy pathways are new potential strategies for re-establishing protein homeostasis and improving heart function. Additionally, lifestyle modifications such as dietary interventions and exercise have been shown to promote cardiac proteostasis and overall metabolic health. The pursuit of future research dedicated to proteostasis and protein quality control represents a pioneering approach for enhancing cardiac health and addressing the complexities of obesity-related cardiac dysfunction.

心血管疾病（CVD）与蛋白质稳态（蛋白质稳态）及其失败密切相关。除了损害心脏蛋白质质量控​​制的基因突变之外，肥胖也是心脏病的一个重要危险因素。在肥胖症中，脂肪组织变得功能失调，并通过释放导致全身胰岛素抵抗和心血管功能障碍的细胞因子来影响心脏功能和心血管疾病进展。此外，慢性炎症和脂毒性会损害内质网（ER）功能，引发应激反应，使蛋白质质量控​​制超出其能力范围。蛋白质稳态受损，包括泛素蛋白酶体系统 (UPS) 功能障碍、自噬和分子伴侣耗竭，与心肌细胞功能障碍有着复杂的联系。针对 UPS 和自噬途径的干预措施是重建蛋白质稳态和改善心脏功能的新的潜在策略。此外，饮食干预和锻炼等生活方式的改变已被证明可以促进心脏蛋白质稳态和整体代谢健康。致力于蛋白质稳态和蛋白质质量控​​制的未来研究代表了增强心脏健康和解决肥胖相关心脏功能障碍复杂性的开创性方法。