Evidence map›Paper›PMID 35741040›Full record

ArticleCells2022

Integrated Analysis Reveals S100a8/a9 Regulates Autophagy and Apoptosis through the MAPK and PI3K-AKT Signaling Pathway in the Early Stage of Myocardial Infarction.

Weijue Yi, Rongli Zhu, Xiuyang Hou, Fengmin Wu, Rui Feng

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Signaling Pathways and Therapeutic Approaches in Post-Myocardial Infarction Fibrosis.Medical science monitor : international medical journal of experimental and clinical research · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. From Cell to Gene: Deciphering the Mechanism of Heart Failure With Single-Cell Sequencing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
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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

5 authors at 1 institution in 1 country.

Weijue YiDepartment of Pharmaceutical Toxicology, School of Pharmacy, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang 110122, China.ORCID 0000-0001-7476-2751
Rongli ZhuDepartment of Pharmaceutical Toxicology, School of Pharmacy, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang 110122, China.
Xiuyang HouDepartment of Pharmaceutical Toxicology, School of Pharmacy, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang 110122, China.ORCID 0000-0002-7545-263X
Fengmin WuDepartment of Pharmaceutical Toxicology, School of Pharmacy, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang 110122, China.ORCID 0000-0002-6688-1432
Rui FengDepartment of Pharmaceutical Toxicology, School of Pharmacy, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang 110122, China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial infarction (MI), a type of coronary heart disease, has had a significantly increased incidence in recent years. The balance of cardiomyocyte apoptosis and autophagy after MI is one of the main determinants of patient prognosis. Both affect myocardial fibrosis and ventricular remodeling and regulate cell survival. However, there are few studies on the regulation mechanism of cardiomyocyte autophagy and apoptosis in the early stage after MI. In this study, based on analyzing the scRNA-seq and mRNA-seq data of mice in the early stage of MI, we found that the expression of S100a8 and S100a9 increased first and then decreased in the early stage of MI, and their expression level changed with the number of neutrophils. Further, through the functional enrichment analysis of the differentially expressed genes, we found that S100a8 and S100a9 were simultaneously associated with autophagy and apoptosis and could regulate autophagy and apoptosis of cardiomyocytes through MAPK or PI3K-AKT signaling pathways. This study provides valuable insights for clarifying the pathogenesis of early stage MI and improving its early treatment.

Indexed as

Myocardial InfarctionProto-Oncogene Proteins c-aktAnimalsApoptosisAutophagyCalgranulin ACalgranulin BHumansMiceMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesSignal TransductionCalgranulin ACalgranulin BMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktS100a8 protein, mouseS100A9 protein, mouseapoptosisautophagymyocardial infarctionS100a8S100a9

Identifiers

PMID35741040
PMCPMC9221389
OpenAlexW4282842018

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.