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Journal article
p62/SQSTM1 at the interface of aging, autophagy, and disease
Age, v 36(3), pp 1123-1137
21 Feb 2014
PMID: 24557832
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Advanced age is characterized by increased incidence of many chronic, noninfectious diseases that impair the quality of living of the elderly and pose a major burden on the healthcare systems of developed countries. These diseases are characterized by impaired or altered function at the tissue and cellular level, which is a hallmark of the aging process. Age-related impairments are likely due to loss of homeostasis at the cellular level, which leads to the accumulation of dysfunctional organelles and damaged macromolecules, such as proteins, lipids, and nucleic acids. Intriguingly, aging and age-related diseases can be delayed by modulating nutrient signaling pathways converging on the target of rapamycin (TOR) kinase, either by genetic or dietary intervention. TOR signaling influences aging through several potential mechanisms, such as autophagy, a degradation pathway that clears the dysfunctional organelles and damaged macromolecules that accumulate with aging. Autophagy substrates are targeted for degradation by associating with p62/SQSTM1, a multidomain protein that interacts with the autophagy machinery. p62/SQSTM1 is involved in several cellular processes, and its loss has been linked to accelerated aging and to age-related pathologies. In this review, we describe p62/SQSTM1, its role in autophagy and in signaling pathways, and its emerging role in aging and age-associated pathologies. Finally, we propose p62/SQSTM1 as a novel target for aging studies and age-extending interventions.
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Details
- Title
- p62/SQSTM1 at the interface of aging, autophagy, and disease
- Creators
- Alessandro Bitto - University of WashingtonChad A. Lerner - University of RochesterTimothy Nacarelli - Drexel UniversityElizabeth Crowe - Drexel UniversityClaudio Torres - Drexel UniversityChristian Sell - Drexel University
- Publication Details
- Age, v 36(3), pp 1123-1137
- Publisher
- Springer Netherlands
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Biochemistry and Molecular Biology; Neurobiology and Anatomy; Pathology (and Laboratory Medicine)
- Web of Science ID
- WOS:000342142300010
- Scopus ID
- 2-s2.0-84905374241
- Other Identifier
- 991019169900804721
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- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Geriatrics & Gerontology