ArticleRedox biology2017
Mitochondrial contribution to lipofuscin formation.
Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 151 citations in OpenAlex.
- The Evaluation of Oxidative Stress Parameters in Serum Patients with Relapsing-Remitting Multiple Sclerosis Treated with II-Line Immunomodulatory Therapy.Oxidative medicine and cellular longevity · 2017Trial
- Lipofuscin: Wear Pigment or Alarm Signal for Cardiac AlloGraft Vasculopathy?Diagnostics (Basel, Switzerland) · 2026Article
- From lipofuscin accumulation to cellular dysfunction: a focus on liver pathophysiology.Histochemistry and cell biology · 2026Review
- Lipofuscin accumulation in aging and CLN1 is associated with deficient de-S-acylation, lyso-mitochondrial dysfunction, and lipid dyshomeostasis.Acta neuropathologica · 2026Article
- Article
- Modification of the dermal matrix by senescence associated lipids and its functional consequence.Redox biology · 2026Article
- Cycloneolitsol prolongs the lifespan of Caenorhabditis elegans by SEK-1/PMK-1/SKN-1 pathway and exerts anti-inflammatory effects by NF-κB pathway.Biogerontology · 2026Article
- Deficient de-S-acylation in aging and CLN1 contributes to lyso-mitochondrial dysfunction, lipid dyshomeostasis, and resultant lipofuscin biogenesis.Research square · 2026Article
- MTFR1L is a cardiac antiaging factor for maintenance of mitochondrial homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Metformin Attenuates Osteoarthritis Progression by Modulating Mitochondrial Dynamics via Activation of the AMPK/Drp1 Pathway.Journal of inflammation research · 2026Article
- Lipofuscin accumulation in aging and neurodegeneration: a potential "timebomb" overlooked in Alzheimer's disease.Translational neurodegeneration · 2025Review
- Inter-Caste Comparison Reveals a Unique Bioenergetic Signature in Long-Lived Ant Queens.Molecular ecology · 2025Article
- Alpha-lipoic acid supplementation improves pathological alterations in cellular models of Friedreich ataxia.Orphanet journal of rare diseases · 2025Article
- sPLA2-IIA modifies progranulin deficiency phenotypes in mouse models.Molecular neurodegeneration · 2025Article
- Article
- AG86 Peptide-modified Reactive Oxygen Species-responsive Polymer Nanovesicles for Transdermal Delivery of Hydrophilic Ergothioneine to Basal Keratinocytes.AAPS PharmSciTech · 2025Article
- Potential of autophagy in subretinal fibrosis in neovascular age-related macular degeneration.Cellular & molecular biology letters · 2025Review
- Oxidized protein aggregate lipofuscin impairs cardiomyocyte contractility via late-stage autophagy inhibition.Redox biology · 2025Article
- Insights into the renal pathophysiology in Hermansky-Pudlak syndrome-1 from urinary extracellular vesicle proteomics and a new mouse model.FEBS letters · 2025Article
- Senolytic treatment to rescue hallmarks of senescence in lymph node fibroblasts from patients with rheumatoid arthritis: Implications for premature aging and potential therapeutic intervention in early rheumatoid arthritis.Clinical and experimental immunology · 2025Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria have been in the focus of oxidative stress and aging research for decades due to their permanent production of ROS during the oxidative phosphorylation. The hypothesis exists that mitochondria are involved in the formation of lipofuscin, an autofluorescent protein aggregate that accumulates progressively over time in lysosomes of post-mitotic and senescent cells. To investigate the influence and involvement of mitochondria in lipofuscinogenesis, we analyzed lipofuscin amounts as well as the mitochondrial function in young and senescent cells. In addition we used an aging model and Lon protease deficient HeLa cells to investigate the influence of mitochondrial degradation processes on lipofuscin formation. We were able to show that mitophagy is impaired in senescent cells resulting in an increased mitochondrial mass and superoxide formation. In addition, the inhibition of mitochondrial fission leads to increased lipofuscin formation. Moreover, we observed that Lon protease downregulation is linked to a higher lipofuscinogenesis whereas the application of the mitochondrial-targeted antioxidant mitoTEMPO is able to prevent the accumulation of this protein aggregate.
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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.