Evidence map›Paper›PMID 33841177›Full record

ReviewFrontiers in physiology2021

The Role of Autophagy in Skeletal Muscle Diseases.

Qianghua Xia, Xubo Huang, Jieru Huang, Yongfeng Zheng, Michael E March, Jin Li, Yongjie Wei

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
11.6field-weighted citation impact, top 1% 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

74 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Metabolomic analyses of amyotrophic lateral sclerosis, muscle cramps, and TJ-68 treatment.Metabolomics : Official journal of the Metabolomic Society · 2026
    Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. HSAInternational journal of molecular sciences · 2025
    Article
  20. Review

14 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

7 authors at 2 institutions in 2 countries.

Qianghua XiaAffiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, China.
Xubo HuangAffiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, China.
Jieru HuangAffiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, China.
Yongfeng ZhengAffiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, China.
Michael E MarchCenter for Applied Genomics, The Children's Hospital of Philadelphia, Philadelphia, PA, United States.
Jin LiAffiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, China.
Yongjie WeiAffiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, China.
Guangzhou Medical University · CNChildren's Hospital of Philadelphia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle is the most abundant type of tissue in human body, being involved in diverse activities and maintaining a finely tuned metabolic balance. Autophagy, characterized by the autophagosome-lysosome system with the involvement of evolutionarily conserved autophagy-related genes, is an important catabolic process and plays an essential role in energy generation and consumption, as well as substance turnover processes in skeletal muscles. Autophagy in skeletal muscles is finely tuned under the tight regulation of diverse signaling pathways, and the autophagy pathway has cross-talk with other pathways to form feedback loops under physiological conditions and metabolic stress. Altered autophagy activity characterized by either increased formation of autophagosomes or inhibition of lysosome-autophagosome fusion can lead to pathological cascades, and mutations in autophagy genes and deregulation of autophagy pathways have been identified as one of the major causes for a variety of skeleton muscle disorders. The advancement of multi-omics techniques enables further understanding of the molecular and biochemical mechanisms underlying the role of autophagy in skeletal muscle disorders, which may yield novel therapeutic targets for these disorders.

Indexed as

AMPKautophagymTORmuscle cell homeostasisskeletal muscle diseasestranscriptional regulation

Identifiers

PMID33841177
PMCPMC8027491
OpenAlexW3149479883

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.