Evidence map›Paper›PMID 30947537›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2019

The protective role of carnosic acid in ischemic/reperfusion injury through regulation of autophagy under T2DM.

Min Hu, Tianyu Li, Zixiang Bo, Feixiang Xiang

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. 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

4 authors at 2 institutions in 1 country.

Min Hu1 Department of Cardiovascular Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Tianyu Li1 Department of Cardiovascular Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Zixiang Bo1 Department of Cardiovascular Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Feixiang Xiang2 Department of Ultrasound, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Huazhong University of Science and Technology · CNTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

impact statementWe have provided, for the first time, evidence that carnosic acid (CA) attenuates ischemia-reperfusion injury of diabetic myocardium, i.e. diabetic myocardial ischemia/reperfusion (DMI/R) injury, via enhancement of autophagy. A greater understanding of the target molecule in CA-enhanced autophagy is necessary for the development of potential chemotherapy for DMI/R injury.

Indexed as

AutophagyAbietanesAMP-Activated Protein Kinase KinasesAnimalsAntioxidantsCells, CulturedCytokinesDiabetes Mellitus, Type 2Diabetic CardiomyopathiesDiet, High-FatMaleMiceMice, Inbred C57BLMicrotubule-Associated ProteinsMyocardial Reperfusion InjuryMyocytes, CardiacAbietanesAMP-Activated Protein Kinase KinasesAntioxidantsCytokinesMAP1LC3A protein, humanMap1lc3b protein, mouseMicrotubule-Associated ProteinsProtein KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciessalvinTOR Serine-Threonine KinasesapoptosisAutophagycarnosic aciddiabetes mellitusinflammationmyocardial ischemia/reperfusion

Identifiers

PMID30947537
PMCPMC6545691
OpenAlexW2930739172

What OpenQuestion 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 OpenQuestion graph.