Dysfunctional mitochondria are a hallmark of T cell ageing and contribute to organismal ageing. This arises from the accumulation of reactive oxygen species (ROS), impaired mitochondrial dynamics, and inefficient removal of dysfunctional mitochondria. Both cell-intrinsic and cell-extrinsic mechanisms for removing mitochondria and their byproducts have been identified in T cells. In this review, we explore how T cells manage mitochondrial damage through changes in mitochondrial metabolism, mitophagy, asymmetric mitochondrial inheritance, and mitochondrial transfer, highlighting the impact of these mechanisms on T cell ageing and overall organismal ageing. We also discuss current therapeutic strategies aimed at removing dysfunctional mitochondria and their byproducts and propose potential new therapeutic targets that may reverse immune ageing or organismal ageing.
Journal article
2025-09-01T00:00:00+00:00
26
4402 - 4418
16
Asymmetric Cell Division, Mitochondrial Metabolism, Mitochondrial Transfer, Mitophagy, T Cell Ageing, Humans, Mitochondria, T-Lymphocytes, Reactive Oxygen Species, Mitophagy, Animals, Aging, Cellular Senescence, Mitochondrial Dynamics