Evidence map›Paper›PMID 35958489›Full record

ArticleAmerican journal of translational research2022

Cryptotanshinone alleviates myocardial ischemia and reperfusion injury in rats to mitigate ER stress-dependent apoptosis by modulating the JAK1/STAT3 axis.

Shasha Wang, Lifang Sun, Zhijian Zhu, Junyi Liu, Wei Ge, Baoyin Li, Bing Wang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

  1. LILRB4 Recruits SHP-1 to Enhance Oxidative Stress and Apoptosis, Aggravating Myocardial Ischemia-Reperfusion Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Expression of PIM1/ASK1 Molecular Pathway Related Genes in Ischemic Cardiomyopathy.Cardiovascular & hematological disorders drug targets · 2025
    Article
  3. Article
  4. 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

7 authors at 1 institution in 1 country.

Shasha WangDepartment of Cardiovascular Medicine, Jinshan Branch of Shanghai Sixth People's Hospital Shanghai 201599, China.
Lifang SunDepartment of Cardiovascular Medicine, Jinshan Branch of Shanghai Sixth People's Hospital Shanghai 201599, China.
Zhijian ZhuDepartment of Cardiovascular Medicine, Jinshan Branch of Shanghai Sixth People's Hospital Shanghai 201599, China.
Junyi LiuDepartment of Cardiovascular Medicine, Jinshan Branch of Shanghai Sixth People's Hospital Shanghai 201599, China.
Wei GeDepartment of Cardiovascular Medicine, Jinshan Branch of Shanghai Sixth People's Hospital Shanghai 201599, China.
Baoyin LiDepartment of Cardiovascular Medicine, Jinshan Branch of Shanghai Sixth People's Hospital Shanghai 201599, China.
Bing WangDepartment of Cardiovascular Medicine, Jinshan Branch of Shanghai Sixth People's Hospital Shanghai 201599, China.
Shanghai Sixth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveMyocardial ischemia is the stoppage or insufficiency of blood flow to the myocardium, depriving cells of oxygen supply which leads to their apoptosis or death. Currently, the management of patients has improved, making it possible to reduce myocardial infarction injury with new strategies of reperfusion and pharmacologic treatment.

methodsA rat model of myocardial ischemia and reperfusion injury (MIRI) was created and subjected to cryptotanshinone (CRY) with or without JAK1 inhibitor filgotinib (FILGO) treatment. H&E staining was used for histopathologic evaluation of heart injury, and TTC staining was employed for evaluation of the infarct size. Western blotting and immunofluorescence were used to measure the protein expression and qRT-PCR for determining mRNA expression.

resultsCRY significantly reduced the area of the infarct, the number of apoptotic cells, and the concentrations of lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) induced by ischemia/reperfusion (I/R). Subsequent analysis showed that CRY repressed the expression of caspase-12, CHOP, and GRP78, but enhanced the phosphorylation of JAK and STAT3. However, FILGO treatment markedly abolished the beneficial effect of CRY pretreatment on cardiomyocyte damage, apoptosis, cardiac function, and inhibition of endoplasmic reticulum stress (ERS)-dependent apoptosis marker proteins.

conclusionCRY may alleviate MIRI by inhibiting ERS-dependent apoptosis by activating the JAK1/STAT3 signaling pathway.

Indexed as

Apoptosiscryptotanshinoneendoplasmic reticulumJAK1/STAT3 signalingmyocardial ischemia and reperfusion injury

Identifiers

PMID35958489
PMCPMC9360873
OpenAlexW4291283521

What Socratic holds

Textmetadata
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 Socratic graph.