Evidence map›Paper›PMID 34007311›Full record

ReviewExperimental and therapeutic medicine2021

The mitochondrial biogenesis signaling pathway is a potential therapeutic target for myasthenia gravis via energy metabolism (Review).

Lingling Ke, Qing Li, Jingwei Song, Wei Jiao, Aidong Ji, Tongkai Chen, Huafeng Pan, Yafang Song

Open access · diamondAbstract readReview
In one paragraph

Review in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. The role of mitochondria in rheumatic diseases.Nature reviews. Rheumatology · 2022
    Review
  15. Article
  16. HSA-miR-34a-5p regulates the SIRT1/TP53 axis in prostate cancer.American journal of translational research · 2022
    Article
  17. International journal of molecular sciences · 2021
    Article
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

8 authors at 1 institution in 1 country.

Lingling KeScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
Qing LiScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
Jingwei SongScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
Wei JiaoScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
Aidong JiClinical Medical College of Acupuncture, Moxibustion and Rehabilitation, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.
Tongkai ChenScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
Huafeng PanScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
Yafang SongScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China.
Guangzhou University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myasthenia gravis (MG) is an autoantibody-mediated autoimmune disease that is characterized by muscle weakness and fatigue. Traditional treatments for MG target the neuromuscular junction (NMJ) or the immune system. However, the efficacy of such treatments is limited, and novel therapeutic options for MG are urgently required. In the current review, a new therapeutic strategy is proposed based on the mitochondrial biogenesis and energy metabolism pathway, as stimulating mitochondrial biogenesis and the energy metabolism might alleviate myasthenia gravis. A number of cellular sensors of the energy metabolism were investigated, including AMP-activated protein kinase (AMPK) and sirtuin 1 (SIRT1). AMPK and SIRT1 are sensors that regulate cellular energy homeostasis and maintain energy metabolism by balancing anabolism and catabolism. Peroxisome proliferator-activated receptor γ coactivator 1α and its downstream transcription factors nuclear respiratory factors 1, nuclear respiratory factors 2, and transcription factor A are key sensors of mitochondrial biogenesis, which can restore mitochondrial DNA and produce new mitochondria. These processes help to control muscle contraction and relieve the symptoms of MG, including muscle weakness caused by dysfunctional NMJ transmission. Therefore, the present review provides evidence for the therapeutic potential of targeting mitochondrial biogenesis for the treatment of MG.

Indexed as

AMP-activated protein kinaseenergy metabolismmitochondriamitochondrial biogenesismyasthenia gravisproliferator-activated receptor γ coactivator 1α

Identifiers

PMID34007311
PMCPMC8120506
OpenAlexW3157650188

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.