Evidence map›Paper›PMID 34668176›Full record

ArticleHistology and histopathology2021

LncRNA TUG1 aggravates cardiomyocyte apoptosis and myocardial ischemia/reperfusion injury.

Dongliang Fu, Tong Gao, Mengru Liu, Chunyan Li, Haiwei Li, Hong Jiang, Xianlun Fu

Abstract read
PubMed Publisher
In one paragraph

Article in Histology and histopathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. LncRNA UCA1 enhances NRF2 expression through the mJournal of bioenergetics and biomembranes · 2024
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. 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.

Dongliang FuCardiology Department of Integrated Traditional Chinese and Western Medicine, China-Japan Friendship Hospital, Beijing, China.
Tong GaoCardiology Department of Integrated Traditional Chinese and Western Medicine, China-Japan Friendship Hospital, Beijing, China.
Mengru LiuCardiology Department of Integrated Traditional Chinese and Western Medicine, China-Japan Friendship Hospital, Beijing, China.
Chunyan LiCardiology Department of Integrated Traditional Chinese and Western Medicine, China-Japan Friendship Hospital, Beijing, China.
Haiwei LiCardiology Department of Integrated Traditional Chinese and Western Medicine, China-Japan Friendship Hospital, Beijing, China.
Hong Jiang *Cardiology Department of Integrated Traditional Chinese and Western Medicine, China-Japan Friendship Hospital, Beijing, China. drjh680@sina.com.
Xianlun Fu *Cardiology Department of Integrated Traditional Chinese and Western Medicine, China-Japan Friendship Hospital, Beijing, China. drjh680@sina.com.
China-Japan Friendship Hospital · CN

Funding

National Natural Science Foundation of China 8167141777
6 · The paper itself

Abstract

Cardiomyocyte apoptosis is a fundamental pathogenic factor leading to myocardial ischemia/reperfusion (MI/R) injury. The long non-coding RNA (IncRNA) TUG1 regulates apoptosis in various cell types. We report here that TUG1 expression is induced in mouse heart following MI/R injury as well as in cardiomyocytes subjected to simulated ischemia/reperfusion (SI/R) in vitro. Clinically, TUG1 expression is also elevated in plasma from patients with acute myocardial infarction (AMI), which implies its potential application as a disease biomarker. Functionally, TUG1 overexpression promotes, and its knockdown reduces SI/R-induced lactate dehydrogenase (LDH) release and caspase-3 activity in cardiomyocytes in vitro, illustrating that TUG1 exacerbates SI/R-induced apoptosis. Furthermore, in vivo, TUG1 aggravates MI/R injury in a mouse model, and subsequent observations show concurrent increased apoptosis of cardiomyocytes. Hence, this study unveils a clinical relevance and functional role of TUG1 in MI/R injury, and also implicates that targeting TUG1 may have therapeutic effects in treating MI/R injury.

Indexed as

AnimalsApoptosisDisease Models, AnimalHumansMiceMice, Inbred C57BLMyocardial InfarctionMyocardial Reperfusion InjuryMyocytes, CardiacRNA, Long Noncodinglong non-coding RNA TUG1, mouseRNA, Long Noncoding

Identifiers

PMID34668176
OpenAlexW3207014278

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.