Recent advances in understanding the mechanisms determining longevity
Open accessAbstract
The field of aging research has progressed significantly over the past decades. Exogenously and endogenously inflicted molecular damage ranging from genotoxic to organellar damage drives the aging process. Repair mechanisms and compensatory responses counteract the detrimental consequences of the various damage types. Here, we discuss recent progress in understanding cellular mechanisms and interconnections between signaling pathways that control longevity. We summarize cell-autonomous and non-cell-autonomous mechanisms that impact the cellular and organismal aging process.
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Many paradigms of life extension depend on autophagy in model organisms (yeast, Drosophila, Caenorhabditis elegans and mice).
“It has been shown in model organisms (yeast, Drosophila, Caenorhabditis elegans and mice) that many paradigms of life extension depend on autophagy [34,130,135,136].”
From The mitochondrial permeability transition: Nexus of aging, disease and longevity (2021) · cites this paper as [34]
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“It has been shown in model organisms (yeast, Drosophila, Caenorhabditis elegans and mice) that many paradigms of life extension depend on autophagy [34,130,135,136].”
BackgroundFundamental Characteristics of Single-Cell Aging in Diploid Yeast
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Evolution of Longevity as a Species-Specific Trait in Mammals
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Liproxstatin-1 Protects SH-SY5Y Cells by Inhibiting H2O2-Induced Excessive Mitophagy and Apoptosis
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- Authors
- Bayersdorf, R., & Schumacher, B.
- Affiliations
- University of Cologne (DE)
- Corresponding author
- Schumacher, Björn
- ORCID
- Schumacher, Björn
- Venue
- F1000Research
- Publisher
- F1000 Research Ltd
- Published
- 2019-08-09
- Volume
- 8
- Pages
- 1403
- ISSN
- 2046-1402 (ISSN-L)
- PMC
- PMC6694448
- OpenAlex
- W2967466257
- Cited by
- 14
- References
- 82
- Citations by year
- 2025: 1 · 2024: 4 · 2022: 1 · 2021: 5 · 2020: 2 · 2018: 1
- FWCI
- 0.17
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- F1000Research (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Deutsche Krebshilfe (70112899)
- Deutsche Forschungsgemeinschaft (SCHU2494/3-1, SCHU2494/7-1, CECAD, SFB829, SFB670, KFO286, KFO329, GRK2407)
- European Cooperation in Science and Technology (BM1408)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- aging, longevity, molecular damage, genetic damage, organelle damage, DNA repair, compensatory response, signaling pathways
- MeSH terms
- Aging, DNA Damage, Humans, Longevity, Signal Transduction
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