Mild overexpression of clpX and clpP resulted in a significant increase in climbing ability during adulthood and a small increase in longevity, suggesting that mild increases in mitochondrial protein degradation, independent of stress response pathway activation, can be sufficient to improve a marker of health and extend lifespan.
Overexpression of Rpt3 enhanced proteasome assembly and activity, reducing intracellular ubiquitin levels in hac1Δ, and upregulates Hac1 protein abundance, thereby ensuring proteostasis maintenance.
Ziting Zhu, Xiaolong Feng, B. Song et al.· The FEBS Journal· 0 citations
It is shown that inhibition of mitochondrial respiration induces a sustained transcriptional program that enhances lysosomal proteolysis during aging in Caenorhabditis elegans and reveals a previously unrecognized ELT-2–dependent lysosomal proteostasis pathway that acts downstream of mitochondrial stress to maintain pr...
Rendan Yang, Yu Sun, Wen-Zheng Wang et al.· Science Advances· 1 citation
This review integrates recent insights into how TLDc proteins coordinate organellar pH regulation and iron homeostasis and discusses how disruption of these interconnected pathways contributes to age-related neurodegeneration.
Mohammad Sajid Ghufran, Priyanka Soni, Bobby Thomas· Redox Biology· 0 citations
Age-linked tissue dysfunction is associated with mitochondrial degeneration manifested as organelle fragmentation and respiratory dysfunction. Efforts to mitigate downstream consequences of mitochondrial degeneration, as with ROS scavengers, have not translated to the human condition. We posit that intrinsic fusion-med...
J. Weigele, Li-Hong Zhang, Jia-Jia Li et al.· Cells· 0 citations
Mitochondria are essential organelles responsible for cellular ATP production and contain their own mitochondrial DNA (mtDNA), which encodes key components of oxidative phosphorylation. Because mitochondria continuously generate reactive oxygen species (ROS), mtDNA is particularly susceptible to oxidative damage. Altho...