Evidence map›Paper›PMID 36968196›Full record

ReviewFrontiers in cell and developmental biology2023

Mitochondrial DNA abnormalities and metabolic syndrome.

Xudong Ding, Tingting Fang, Xiaoqi Pang, Xueru Pan, Aiying Tong, Ziyi Lin, Shikuan Zheng, Ningning Zheng

Open access · goldFull text readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Mitochondrial tRNA-Derived Diseases.International journal of molecular sciences · 2025
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Mitochondrial Dysfunction in Diabetes: Shedding Light on a Widespread Oversight.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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.

Xudong DingDepartment of Anesthesiology, Shengjing Hospital, China Medical University, Liaoning, China.
Tingting FangDepartment of Pathophysiology, College of Basic Medical Science, China Medical University, Liaoning, China.
Xiaoqi PangShengjing Hospital, China Medical University, Liaoning, China.
Xueru PanPharmaceutical Sciences, China Medical University-The Queen's University of Belfast Joint College, China Medical University, Liaoning, China.
Aiying TongPharmaceutical Sciences, China Medical University-The Queen's University of Belfast Joint College, China Medical University, Liaoning, China.
Ziyi LinPharmaceutical Sciences, China Medical University-The Queen's University of Belfast Joint College, China Medical University, Liaoning, China.
Shikuan ZhengPharmaceutical Sciences, China Medical University-The Queen's University of Belfast Joint College, China Medical University, Liaoning, China.
Ningning ZhengDepartment of Pathophysiology, College of Basic Medical Science, China Medical University, Liaoning, China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic syndrome (MetS) is a complex pathological condition that involves disrupted carbohydrate, protein, and fat metabolism in the human body, and is a major risk factor for several chronic diseases, including diabetes, cardiovascular disease, and cerebrovascular disease. While the exact pathogenesis of metabolic syndrome is not yet fully understood, there is increasing evidence linking mitochondrial dysfunction, which is closely related to the mitochondrial genome and mitochondrial dynamics, to the development of this condition. Recent advancements in genetic sequencing technologies have allowed for more accurate detection of mtDNA mutations and other mitochondrial abnormalities, leading to earlier diagnosis and intervention in patients with metabolic syndrome. Additionally, the identification of specific mechanisms by which reduced mtDNA copy number and gene mutations, as well as abnormalities in mtDNA-encoded proteins and mitochondrial dynamics, contribute to metabolic syndrome may promote the development of novel therapeutic targets and interventions, such as the restoration of mitochondrial function through the targeting of specific mitochondrial defects. Additionally, advancements in genetic sequencing technologies may allow for more accurate detection of mtDNA mutations and other mitochondrial abnormalities, leading to earlier diagnosis and intervention in patients with MetS. Therefore, strategies to promote the restoration of mitochondrial function by addressing these defects may offer new options for treating MetS. This review provides an overview of the research progress and significance of mitochondrial genome and mitochondrial dynamics in MetS.

Indexed as

metabolic syndromemitochondrial copy numbermitochondrial dynamicsmitochondrial-encoded proteinsmitochondrial gene mutationsmitochondrial proteases

Identifiers

PMID36968196
PMCPMC10036395
OpenAlexW4323858338

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read9
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.