Caveolin-1, cellular senescence and age-related diseases.
Caveolin-1, cellular senescence and age-related diseases.
复制标题
DOI：
10.1016/j.mad.2011.11.001
复制
发表时间：
2011-11
影响因子：
5.3
通讯作者：
Galbiati F
中科院分区：
文献类型：
--
作者：
Zou H;Stoppani E;Volonte D;Galbiati F
根据衰老的“自由基理论”，正常衰老是由于活性氧（ROS）产生超过细胞抗氧化能力时造成组织损伤的结果。 ROS 会引起细胞功能障碍，例如应激诱导的早衰 (SIPS)，这被认为会导致正常的机体衰老，并在与年龄相关的疾病中发挥作用。与这一假设相一致的是，老年动物中 DNA、蛋白质和脂质的氧化损伤增加，并且随着年龄的增长，衰老细胞在体内积累。 Caveolin-1 作为一种支架蛋白，可集中信号分子并对其进行功能性调节。最近，在了解 Caveolin-1 在应激诱导的过早衰老中的作用方面取得了巨大进展。数据显示，小窝蛋白介导的信号传导可能有助于在分子水平上解释氧化应激如何促进细胞衰老的有害影响，例如衰老和与年龄相关的疾病。在这篇综述中，我们讨论了 SIPS 背景下 Caveolin-1 的细胞机制和功能及其与衰老生物学的相关性。
According to the “free radical theory” of aging, normal aging occurs as the result of tissue damages inflicted by reactive oxygen species (ROS) when ROS production exceeds the antioxidant capacity of the cell. ROS induce cellular dysfunctions such as stress-induced premature senescence (SIPS), which is believed to contribute to normal organismal aging and play a role in age-related diseases. Consistent with this hypothesis, increased oxidative damage of DNA, proteins, and lipids have been reported in aged animals and senescent cells accumulate in vivo with advancing age. Caveolin-1 acts as a scaffolding protein that concentrates and functionally regulates signaling molecules. Recently, great progress has been made toward understanding of the role of caveolin-1 in stress-induced premature senescence. Data show that caveolin-mediated signaling may contribute to explain, at the molecular level, how oxidative stress promotes the deleterious effects of cellular senescence such as aging and age-related diseases. In this review, we discuss the cellular mechanisms and functions of caveolin-1 in the context of SIPS and their relevance to the biology of aging.