The role of mitochondria in cytokine and chemokine signalling during ageing.
Abstract
Ageing is accompanied by a persistent, low-level inflammation, termed "inflammageing", which contributes to the pathogenesis of age-related diseases. Mitochondria fulfil multiple roles in host immune responses, while mitochondrial dysfunction, a hallmark of ageing, has been shown to promote chronic inflammatory states by regulating the production of cytokines and chemokines. In this review, we aim to disentangle the molecular mechanisms underlying this process. We describe the role of mitochondrial signalling components such as mitochondrial DNA, mitochondrial RNA, N-formylated peptides, ROS, cardiolipin, cytochrome c, mitochondrial metabolites, potassium efflux and mitochondrial calcium in the age-related immune system activation. Furthermore, we discuss the effect of age-related decline in mitochondrial quality control mechanisms, including mitochondrial biogenesis, dynamics, mitophagy and UPR
The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.
Research summary
The paper discusses the role of mitochondria in the context of inflammageing and its contribution to age-related diseases, focusing on the molecular mechanisms that underlie these processes. This aligns with longevity research as it addresses mitochondrial dysfunction, a key factor in the aging process. However, while the review provides solid insights into mitochondrial signalling and its implications for inflammation during aging, it does not present groundbreaking findings or novel interventions that could significantly advance the field, thus warranting a moderate impact score.
Author of this paper? Send a correction.