ArticleCell communication and signaling : CCS2022
Catalase-deficient mice induce aging faster through lysosomal dysfunction.
Article in Cell communication and signaling : CCS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Organellar insights in ageing and longevity.Nature cell biology · 2026Review
- Mitochondrial dysfunction in cellular senescence: a bridge to neurodegenerative disease.npj aging · 2025Review
- Lysosome as a Chemical Reactor.International journal of molecular sciences · 2025Review
- The impact of aging on liver health and the development of liver diseases.Hepatology communications · 2025Review
- Beyond Antioxidants: How Redox Pathways Shape Cellular Signaling and Disease Outcomes.Antioxidants (Basel, Switzerland) · 2025Review
- Mitochondrial dysfunction in the regulation of aging and aging-related diseases.Cell communication and signaling : CCS · 2025Review
- PLK3 weakens antioxidant defense and inhibits proliferation of porcine Leydig cells under oxidative stress.Scientific reports · 2025Article
- Senescence-associated 13-HODE production promotes age-related liver steatosis by directly inhibiting catalase activity.Nature communications · 2023Article
- Lysosomes in senescence and aging.EMBO reports · 2023Review
- Three Major Causes of Metabolic Retinal Degenerations and Three Ways to Avoid Them.International journal of molecular sciences · 2023Review
- Enhanced Levels of Peroxisome-Derived HAntioxidants (Basel, Switzerland) · 2023Article
- Ameliorative effect of black tea extract on the skin of D-galactose-induced aging mice.Frontiers in nutrition · 2023Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLysosomes are a central hub for cellular metabolism and are involved in the regulation of cell homeostasis through the degradation or recycling of unwanted or dysfunctional organelles through the autophagy pathway. Catalase, a peroxisomal enzyme, plays an important role in cellular antioxidant defense by decomposing hydrogen peroxide into water and oxygen. In accordance with pleiotropic significance, both impaired lysosomes and catalase have been linked to many age-related pathologies with a decline in lifespan. Aging is characterized by progressive accumulation of macromolecular damage and the production of high levels of reactive oxygen species. Although lysosomes degrade the most long-lived proteins and organelles via the autophagic pathway, the role of lysosomes and their effect on catalase during aging is not known. The present study investigated the role of catalase and lysosomal function in catalase-knockout (KO) mice.
methodsWe performed experiments on WT and catalase KO younger (9 weeks) and mature adult (53 weeks) male mice and Mouse embryonic fibroblasts isolated from WT and KO mice from E13.5 embryos as in vivo and in ex-vivo respectively. Mouse phenotyping studies were performed with controls, and a minimum of two independent experiments were performed with more than five mice in each group.
resultsWe found that at the age of 53 weeks (mature adult), catalase-KO mice exhibited an aging phenotype faster than wild-type (WT) mice. We also found that mature adult catalase-KO mice induced leaky lysosome by progressive accumulation of lysosomal content, such as cathespin D, into the cytosol. Leaky lysosomes inhibited autophagosome formation and triggered impaired autophagy. The dysregulation of autophagy triggered mTORC1 (mechanistic target of rapamycin complex 1) activation. However, the antioxidant N-acetyl-L-cysteine and mTORC1 inhibitor rapamycin rescued leaky lysosomes and aging phenotypes in catalase-deficient mature adult mice.
conclusionsThis study unveils the new role of catalase and its role in lysosomal function during aging. Video abstract.
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