Evidence map›Paper›PMID 33608813›Full record

ReviewGeroScience2021

Implication of post-translationally modified SOD1 in pathological aging.

Kashfia Shafiq, Nitesh Sanghai, Ying Guo, Jiming Kong

Open access · greenAbstract readReview
In one paragraph

Review in GeroScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Daily intake of antioxidants ameliorates PMFrontiers in nutrition · 2026
    Article
  5. Review
  6. Article
  7. International journal of molecular sciences · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Therapeutic role of neural stem cells in neurological diseases.Frontiers in bioengineering and biotechnology · 2024
    Review
  13. Review
  14. Article
  15. Identification of Small Airway Epithelium-Related Hub Genes in Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2022
    Article
  16. Review
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

4 authors at 3 institutions in 2 countries.

Kashfia ShafiqDepartment of Human Anatomy and Cell Science, Rady Faculty of Health Science, University of Manitoba, Winnipeg, MB, R3E 0J9, Canada.
Nitesh SanghaiCollege of Pharmacy, Rady Faculty of Health Science, University of Manitoba, Winnipeg, MB, R3E 0T5, Canada.
Ying GuoDepartment of Human Anatomy and Cell Science, Rady Faculty of Health Science, University of Manitoba, Winnipeg, MB, R3E 0J9, Canada.
Jiming KongDepartment of Human Anatomy and Cell Science, Rady Faculty of Health Science, University of Manitoba, Winnipeg, MB, R3E 0J9, Canada. Jiming.Kong@umanitoba.ca.ORCID http://orcid.org/0000-0002-2859-9831
University of Manitoba · CACanada Research Chairs · CAHebei North University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Why certain people relish healthy aging throughout their life span while others suffer pathological consequences? In this review, we focus on some of the dominant paradigms of pathological aging, such as amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD), and Parkinson's disease (PD), and predict that the antioxidant superoxide dismutase 1 (SOD1), when post-translationally modified by aging-associated oxidative stress, acts as a mechanism to accelerated aging in these age-related neurodegenerative diseases. Oxidative modifications of natively reduced SOD1 induce pathological confirmations such as misfolding, leading to a subsequent formation of monomeric, oligomeric, and multimeric aggregates. Misfolded SOD1 propagates like prions from cell to cell. These modified conformations are detected in brain tissues in ALS, AD, and PD, and are considered a contributing factor to their initial pathogenesis. We have also elaborated on oxidative stress-induced non-native modifications of SOD1 and offered a logistic argument on their global implication in accelerated or pathological aging in the context of ALS, AD, and PD.

Indexed as

Amyotrophic Lateral SclerosisParkinson DiseaseProtein Processing, Post-TranslationalAgingHumansProtein FoldingSuperoxide Dismutase-1SOD1 protein, humanSuperoxide Dismutase-1Alzheimer’s disease (AD)Amyotrophic lateral sclerosis (ALS)Oxidative stressParkinson’s disease (PD)Pathological agingPost-translational modificationSOD1

Identifiers

PMID33608813
PMCPMC8110659
OpenAlexW3132110159

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.