Article

Prolonged disturbance of proteostasis induces cellular senescence via temporal mitochondrial dysfunction and enhanced mitochondrial biogenesis in human fibroblasts

2020-01-23

Abstract excerpt

Proteolytic activities decline with age, resulting in the accumulation of aggregated proteins in aged organisms. To investigate how disturbance in proteostasis causes cellular senescence, we developed a stress-induced premature senescence (SIPS) model, in which normal human fibroblast MRC-5 cells were treated with either the proteasome inhibitor MG132 or the V-ATPase inhibitor bafilomycin A1 (BAFA1) for 5 days. Ti...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: d9ba8da0-ff50-52ce-aac2-8a264a7a32b4
DOI: 10.1101/2020.01.22.916221

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

Prolonged disturbance of proteostasis induces cellular senescence via temporal mitochondrial dysfunction and enhanced mitochondrial biogenesis in human fibroblastsDOI 10.1101/2020.01.22.916221Read

Suppressed basal mitophagy drives cellular aging phenotypes that can be reversed by a p62-targeting small molecule.Semantic proximity Read

SIPS as a model to study age-related changes in proteolysis and aggregate formationSemantic proximity Read

Accumulation of damaged mitochondria in aging astrocytes due to mitophagy dysfunction: Implications for susceptibility to mitochondrial stressSemantic proximity Read

Proteostasis failure and mitochondrial dysfunction leads to aneuploidy-induced senescenceSemantic proximity Read

Mitochondrial respiratory dysfunction-elicited oxidative stress and posttranslational protein modification in mitochondrial diseases.Semantic proximity Read

Downregulated miR-181a alleviates H2O2-induced oxidative stress and cellular senescence by targeting PDIA6 in human foreskin fibroblastsSemantic proximity Read

Proteasome dysfunction in<i>Drosophila</i>signals to an Nrf2-dependent regulatory circuit aiming to restore proteostasis and prevent premature agingSemantic proximity Read

Monoamine oxidase-A is a novel driver of stress-induced premature senescence through inhibition of parkin-mediated mitophagy.Semantic proximity Read

Protein oxidation and degradation during proliferative senescence of human MRC-5 fibroblastsSemantic proximity Read

Small molecular antioxidants effectively protect from PUVA-induced oxidative stress responses underlying fibroblast senescence and photoaging.Semantic proximity Read

Autophagy Impairment Induces Premature Senescence in Primary Human FibroblastsSemantic proximity Read

Mitochondrial Dysfunction and Protein Homeostasis in Aging: Insights from a Premature-Aging Mouse ModelSemantic proximity Read