Evidence map›Paper›PMID 34858041›Full record

ReviewDiabetes, metabolic syndrome and obesity : targets and therapy2021

Mitophagy Disequilibrium, a Prominent Pathological Mechanism in Metabolic Heart Diseases.

Yunhao Li, Ningning Zheng, Xudong Ding

Open access · goldAbstract readReview
In one paragraph

Review in Diabetes, metabolic syndrome and obesity : targets and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.7field-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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Mitophagy in metabolic syndrome.Journal of clinical hypertension (Greenwich, Conn.) · 2023
    Review
  9. The Role of Mitochondria in Metabolic Syndrome-Associated Cardiomyopathy.Oxidative medicine and cellular longevity · 2022
    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

3 authors at 2 institutions in 1 country.

Yunhao Li *The First Clinical College, China Medical University, Shenyang, Liaoning, People's Republic of China.ORCID 0000-0002-5359-2930
Ningning Zheng *Department of Pathophysiology, College of Basic Medical Science, China Medical University, Shenyang, Liaoning, People's Republic of China.ORCID 0000-0002-9728-2651
Xudong DingDepartment of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China.ORCID 0000-0002-7204-0007
China Medical University · CNAffiliated Hospital of Liaoning University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

With overall food intake among the general population as high as ever, metabolic syndrome (MetS) has become a global epidemic and is responsible for many serious life-threatening diseases, especially heart failure. In multiple metabolic disorders, maintaining a dynamic balance of mitochondrial number and function is necessary to prevent the overproduction of reactive oxygen species (ROS), which has been proved to be one of the important mechanisms of cardiomyocyte injury due to the mismatching of oxygen consumption and mitochondrial population and finally to heart failure. Mitophagy is a process that eliminates damaged or redundant mitochondria. It is mediated by a series of signaling molecules, including PINK, parkin, BINP3, FUNDC1, CTSD, Drp1, Rab9 and mTOR. Meanwhile, increasing evidence also showed that the interaction between ferroptosis and mitophagy interfered with mitochondrial homeostasis. This review will focus on these essential molecules and pathways of mitophagy and cell homeostasis affected by hypoxia and other stimuli in metabolic heart diseases.

Indexed as

Bcl-2/E1B19kDa-interacting proteinBNIP3ferroptosisFUN14 domain-containing protein 1FUNDC1metabolic heart diseasesmetabolic syndromemitophagyparkinPINKPTEN induced putative kinase

Identifiers

PMID34858041
PMCPMC8629916
OpenAlexW3217364631

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.