Salmonowicz Hanna, Szczepanowska Karolina
IMol Polish Academy of Sciences, 02-247 Warsaw, Poland; Remedy International Research Agenda Unit, IMol Polish Academy of Sciences, 02-247 Warsaw, Poland.
IMol Polish Academy of Sciences, 02-247 Warsaw, Poland; Remedy International Research Agenda Unit, IMol Polish Academy of Sciences, 02-247 Warsaw, Poland.
Trends Cell Biol. 2025 Mar 26. doi: 10.1016/j.tcb.2025.02.008.
While mitochondrial dysfunction is one of the canonical hallmarks of aging, it remains only vaguely defined. Its core feature embraces defects in energy-producing molecular machinery, the mitochondrial respiratory complexes (MRCs). The causes and consequences of these defects hold research attention. In this review, we assess the lifecycle of respiratory complexes, from biogenesis to degradation, and look closely at the mechanisms that could underpin their dysfunction in aged cells. We discuss how these processes could be altered by aging and expand on the fate of MRCs in age-associated pathologies. Given the complexity behind MRC maintenance and functionality, several traits could contribute to the phenomenon known as age-associated mitochondrial dysfunction. New advances will help us better understand the fate of this machinery in aging and age-related diseases.
虽然线粒体功能障碍是衰老的典型特征之一,但其定义仍很模糊。其核心特征包括产生能量的分子机制——线粒体呼吸链复合物(MRCs)存在缺陷。这些缺陷的原因和后果备受研究关注。在本综述中,我们评估呼吸链复合物从生物发生到降解的生命周期,并仔细研究可能导致其在衰老细胞中功能障碍的机制。我们讨论衰老如何改变这些过程,并详述MRCs在与年龄相关的病理状态下的命运。鉴于MRC维持和功能背后的复杂性,多种特性可能导致所谓的与年龄相关的线粒体功能障碍现象。新进展将帮助我们更好地理解这种机制在衰老及与年龄相关疾病中的命运。