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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Chondrogianni, Niki Georgila, Konstantina Kourtis, Nikos Tavernarakis, Nektarios Gonos Efstathios, S. |
| Description | Country affiliation: Greece Author Affiliation: Chondrogianni N ( National Hellenic Research Foundation (Institute of Biology, Medicinal Chemistry & Biotechnology), Greece.); Georgila K ( National Hellenic Research Foundation (Institute of Biology, Medicinal Chemistry & Biotechnology), Greece.); Kourtis N ( Foundation of Research & Technology Hellas (Institute of Molecular Biology & Biotechnology), Greece.); Tavernarakis N ( Foundation of Research & Technology Hellas (Institute of Molecular Biology & Biotechnology), Greece.); Gonos Efstathios S ( National Hellenic Research Foundation (Institute of Biology, Medicinal Chemistry & Biotechnology), Greece.) |
| Abstract | Collapse of proteostasis and accumulation of damaged macromolecules have been recognized as hallmarks of aging and age-related diseases. The proteasome is the major cellular protease responsible for intracellular protein degradation, having an impaired function during aging. We have previously shown that proteasome activation through overexpression of ß5 proteasome subunit delays replicative senescence and confers resistance to oxidative stress in primary fibroblasts. Herein, we have investigated the impact of enhanced proteasome function on organismal longevity and aggregation-related pathologies by employing Caenorhabditis elegans as a model system. We have found that overexpression of a core 20S proteasome subunit in wild type worms extends lifespan, healthspan and survival under proteotoxic conditions. The longevity prolonging effect of the proteasome subunit overexpression was found to depend on the FOXO transcription factor DAF-16 and was associated with its elevated transcriptional activity. We have also uncovered a major role of enhanced proteasome activity in aggregation-related pathologies underlying neurodegenerative diseases. Genetic activation of the proteasome minimized the detrimental effect of polyglutamine-induced toxicity mimicking Huntington's disease, whereas knock-down of the proteasome component exaggerated the disease phenotypes. Similar results were obtained by using a C.elegans model of Amyloid beta (Αß) -induced toxicity mimicking Alzheimer's disease. Collectively, these findings demonstrate that enhanced proteasome function alleviates proteotoxicity and promotes longevity in synergy with other nodes of lifespan regulation in C.elegans. Understanding the mechanism by which preservation of proteostasis via enhancement of proteasome function, decelerates the aging process and alleviates age-related pathologies may assist in the rational design of therapeutic and anti-aging interventions. |
| File Format | HTM / HTML |
| ISSN | 08915849 |
| Issue Number | Suppl 1 |
| Journal | Free Radical Biology and Medicine |
| Volume Number | 75 |
| e-ISSN | 18734596 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2014-10-01 |
| Publisher Place | United States |
| Access Restriction | One Nation One Subscription (ONOS) |
| Content Type | Text |
| Resource Type | Article |
| Subject | Physiology (medical) Biochemistry |
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