ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2011
Impairment of lon-induced protection against the accumulation of oxidized proteins in senescent wi-38 fibroblasts.
Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 58 citations in OpenAlex.
- Lon-dependent proteolysis in oxidative stress responses.Journal of bacteriology · 2025Review
- Mitochondrial dynamics and quality control regulate proteostasis in neuronal ischemia-reperfusion.Autophagy · 2025Article
- YME1L-mediated mitophagy protects renal tubular cells against cellular senescence under diabetic conditions.Biological research · 2024Article
- In Silico and In Vivo Pharmacokinetic Evaluation of 84-B10, a Novel Drug Candidate against Acute Kidney Injury and Chronic Kidney Disease.Molecules (Basel, Switzerland) · 2023Article
- LONP1 targets HMGCS2 to protect mitochondrial function and attenuate chronic kidney disease.EMBO molecular medicine · 2023Article
- Mitochondrial Unfolded Protein Responses in White Adipose Tissue: Lipoatrophy, Whole-Body Metabolism and Lifespan.International journal of molecular sciences · 2021Review
- The Mitochondrial Lon Protease: Novel Functions off the Beaten Track?Biomolecules · 2020Review
- Limitations to adaptive homeostasis in an hyperoxia-induced model of accelerated ageing.Redox biology · 2019Article
- Mitochondria organize the cellular proteostatic response and promote cellular senescence.Cell stress · 2019Article
- Bi-allelic mutations of LONP1 encoding the mitochondrial LonP1 protease cause pyruvate dehydrogenase deficiency and profound neurodegeneration with progressive cerebellar atrophy.Human molecular genetics · 2019Article
- Mitochondrial Dysfunctions: A Thread Sewing Together Alzheimer's Disease, Diabetes, and Obesity.Oxidative medicine and cellular longevity · 2019Review
- To adapt or not to adapt: Consequences of declining Adaptive Homeostasis and Proteostasis with age.Mechanisms of ageing and development · 2019Review
- The mitochondrial unfolded protein response and mitohormesis: a perspective on metabolic diseasesJournal of molecular endocrinology · 2018Review
- Adaptive homeostasis and the free radical theory of ageing.Free radical biology & medicine · 2018Review
- Aging attenuates redox adaptive homeostasis and proteostasis in female mice exposed to traffic-derived nanoparticles ('vehicular smog').Free radical biology & medicine · 2018Article
- Sexual Dimorphism and Aging Differentially Regulate Adaptive Homeostasis.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018Article
- Redox Regulation of Homeostasis and Proteostasis in Peroxisomes.Physiological reviews · 2018Review
- The role of declining adaptive homeostasis in ageing.The Journal of physiology · 2017Review
- Sexual dimorphism in oxidant-induced adaptive homeostasis in multiple wild-type D. melanogaster strains.Archives of biochemistry and biophysics · 2017Article
- The peroxisomal Lon protease LonP2 in aging and disease: functions and comparisons with mitochondrial Lon protease LonP1.Biological reviews of the Cambridge Philosophical Society · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Oxidative damage to mitochondrial proteins is thought to contribute to the aging process, but the Lon protease normally degrades such proteins. In early-passage WI-38 human lung fibroblasts, Lon expression is rapidly induced during H(2)O(2) stress, which prevents the accumulation of oxidized proteins and protects cell viability. In contrast, middle passage cells exhibit only sluggish induction of Lon expression in oxidative stress, and oxidized proteins initially accumulate. Late-passage, or senescent, cells have low basal levels of Lon and high levels of accumulated oxidized proteins; in response to oxidative stress, they fail to induce Lon expression and exhibit continually increasing accumulation of oxidized proteins. Senescent cells separated into two populations, one exhibiting normal mitochondrial mass and a second displaying significant loss of mitochondria; both populations had diminished mitochondrial transmembrane potential. These senescent changes are similar to the effects of Lon silencing in young cells. We suggest that loss of Lon stress inducibility is part of a pattern of diminishing stress adaptability that predisposes cells to senescence.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.