Evidence map›Paper›PMID 24557832›Full record

ReviewAge (Dordrecht, Netherlands)2014

P62/SQSTM1 at the interface of aging, autophagy, and disease.

Alessandro Bitto, Chad A Lerner, Timothy Nacarelli, Elizabeth Crowe, Claudio Torres, Christian Sell

Open access · bronzeAbstract readReview
In one paragraph

Review in Age (Dordrecht, Netherlands), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
8.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

79 citing papers in PubMed, 147 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. The Roles of SQSTM1/p62 in Selective Autophagy and Oncogenic Signaling.International journal of molecular sciences · 2026
    Review
  5. Telomeric autophagy in human health, aging, and diseases.Frontiers in molecular biosciences · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. PAHSAs reduce cellular senescence and protect pancreatic beta cells from metabolic stress through regulation of Mdm2/p53.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  18. Article
  19. Article
  20. Article

19 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Alessandro BittoDepartment of Pathology, University of Washington, Health Science Building D-514, Box 357470, Seattle, WA, USA.
Chad A Lerner
Timothy Nacarelli
Elizabeth Crowe
Claudio Torres
Christian Sell
Drexel University · USUniversity of Rochester · USUniversity of Washington · US

Funding

Role of IGF-1 in Modulation of LongevityR01AG022443 · NIA · LANKENAU INSTITUTE FOR MEDICAL RESEARCH · PI SELL, CHRISTIAN · 2005 to 2009
$1.7M
Novel models for longevity researchR21AG039799 · NIA · DREXEL UNIVERSITY · PI SELL, CHRISTIAN · 2011 to 2012
$425k
Astrocyte senescence and HIV-associated neurocognitive disordersF30AG043307 · NIA · DREXEL UNIVERSITY · PI CROWE, ELIZABETH PATRICIA · 2012 to 2015
$190k
6 · The paper itself

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.

Indexed as

Gene Expression Regulation, DevelopmentalAdaptor Proteins, Signal TransducingAgingAutophagyDNAHumansImmediate-Early ProteinsSequestosome-1 ProteinSignal TransductionAdaptor Proteins, Signal TransducingDNAImmediate-Early ProteinsSequestosome-1 ProteinSQSTM1 protein, human

Identifiers

PMID24557832
PMCPMC4082582
OpenAlexW2039874643

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.