在大鼠、猴子和果蝇的心脏内，纽带蛋白会随着年龄的增长而积累，它能帮助心脏维持功能，并在某些情况下延长寿命。Gaurav Kaushik和同事证明，纽带蛋白在猴子和大鼠心脏内的产生会随着年龄而增加，从而强化心肌并改善个体心肌细胞的收缩能力。他们提出，在没有新细胞再生的情况下，这种类型的心肌细胞重构可维持较年长心脏的跳动与健康。目前还没有用纽带蛋白进行治疗的临床试验，但该蛋白可能是一个有潜力的治疗老化相关性心脏衰竭(这种疾病在全世界正在增加)的候选药物。纽带蛋白是一种细胞结构蛋白，它位于细胞相遇的地方，并附着在与控制细胞运动和形状的丝状“骨架”相连的蛋白簇中。Kaushik和同事发现，在年迈果蝇体内的纽带蛋白会在心肌内细胞与细胞间的接合点处积聚，在这些接合点处，纽带蛋白或能帮助加固心肌纤维并补偿老年心肌细胞变弱的收缩力传输。研究人员还注意到，那些在心脏中过度表达纽带蛋白的果蝇其寿命平均延长了150%。在一则相关的《焦点》文章中，Kristine Y. DeLeon-Pennell 和 Merry L. Lindsey讨论了这些跨物种蛋白组学分析的能力以及纽带蛋白浓度是否在未来能被用作人类心脏老化或衰竭的标记。
纽带蛋白会随着我们年龄增长而在心脏中积聚，它能帮助强化心脏结构并改善心肌细胞的收缩能力。研究人员在果蝇、大鼠和猴子中对纽带蛋白进行了研究，他们说，该蛋白可在无需产生新的心肌细胞情况下重建年老的心脏并维持其健康。
原文链接：Vinculin network–mediated cytoskeletal remodeling regulates contractile function in the aging heart
原文摘要：The human heart is capable of functioning for decades despite minimal cell turnover or regeneration, suggesting that molecular alterations help sustain heart function with age. However, identification of compensatory remodeling events in the aging heart remains elusive. We present the cardiac proteomes of young and old rhesus monkeys and rats, from which we show that certain age-associated remodeling events within the cardiomyocyte cytoskeleton are highly conserved and beneficial rather than deleterious. Targeted transcriptomic analysis in Drosophilaconfirmed conservation and implicated vinculin as a unique molecular regulator of cardiac function during aging. Cardiac-restricted vinculin overexpression reinforced the cortical cytoskeleton and enhanced myofilament organization, leading to improved contractility and hemodynamic stress tolerance in healthy and myosin-deficient fly hearts. Moreover, cardiac-specific vinculin overexpression increased median life span by more than 150% in flies. A broad array of potential therapeutic targets and regulators of age-associated modifications, specifically for vinculin, are presented. These findings suggest that the heart has molecular mechanisms to sustain performance and promote longevity, which may be assisted by therapeutic intervention to ameliorate the decline of function in aging patient hearts.
