Evidence map›Paper›PMID 31967865›Full record

ArticleBiochemistry and cell biology = Biochimie et biologie cellulaire2020

Exogenous ubiquitin attenuates hypoxia/reoxygenation-induced cardiac myocyte apoptosis via the involvement of CXCR4 and modulation of mitochondrial homeostasis.

Suman Dalal, Christopher R Daniels, Ying Li, Gary L Wright, Mahipal Singh, Krishna Singh

Open access · greenAbstract read
In one paragraph

Article in Biochemistry and cell biology = Biochimie et biologie cellulaire, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Almost 50 Years of Monomeric Extracellular Ubiquitin (eUb).Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Cardioprotective Potential of Exogenous Ubiquitin.Cardiovascular drugs and therapy · 2021
    Review
  9. Review
  10. 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

6 authors at 2 institutions in 1 country.

Suman DalalDepartment of Biomedical Sciences, James H Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA.
Christopher R DanielsDepartment of Biomedical Sciences, James H Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA.
Ying LiDepartment of Biomedical Sciences, James H Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA.
Gary L WrightDepartment of Biomedical Sciences, James H Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA.
Mahipal SinghDepartment of Biomedical Sciences, James H Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA.
Krishna SinghDepartment of Biomedical Sciences, James H Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA.
East Tennessee State University · USJames H. Quillen VA Medical Center · US

Funding

Cardioprotective Role of Extracellular Ubiquitin in Myocardial Ischemia/Reperfusion Injury and Myocyte ApoptosisR15HL141947 · NHLBI · EAST TENNESSEE STATE UNIVERSITY · PI SINGH, MAHIPAL · 2018 to 2018
$425k
Role of ATM in Myocardial Remodeling following Myocardial InfarctionR15HL129140 · NHLBI · EAST TENNESSEE STATE UNIVERSITY · PI SINGH, MAHIPAL · 2015 to 2015
$423k
ER stress: role in myocyte apoptosis and myocardial remodelingI01BX000640 · VA · JAMES H QUILLEN VA MEDICAL CENTER · PI SINGH, KRISHNA · 2011 to 2013
–
Osteopontin: role in myocyte apoptosis and myocardial functionI01BX002332 · VA · JAMES H QUILLEN VA MEDICAL CENTER · PI SINGH, KRISHNA · 2014 to 2017
–
Investigation of therapeutic potential of exogenous ubiquitin following myocardial ischemia/reperfusion injuryI01BX004045 · VA · JAMES H QUILLEN VA MEDICAL CENTER · PI SINGH, KRISHNA · 2019 to 2025
–
BLRD VA I01 BX000640BLRD VA I01 BX002332BLRD VA I01 BX004045NHLBI NIH HHS R15 HL129140NHLBI NIH HHS R15 HL141947
6 · The paper itself

Abstract

Exogenous ubiquitin (UB) plays a protective role in β-adrenergic receptor-stimulated and ischemia/reperfusion (I/R)-induced myocardial remodeling. Here, we report that UB treatment inhibits hypoxia/reoxygenation (H/R)-induced apoptosis in adult rat ventricular myocytes (ARVMs). The activation of Akt was elevated, whereas the activation of glycogen synthase kinase-3β was reduced in UB-treated cells post-H/R. The level of oxidative stress was lower, whereas the number of ARVMs with polarized mitochondria was significantly greater in the UB-treated samples. ARVMs express CXCR4 with majority of CXCR4 localized in the membrane fraction. CXCR4 antagonism using AMD3100, and siRNA-mediated knockdown of CXCR4 negated the protective effects of UB. Two mutated UB proteins (unable to bind CXCR4) had no effect on H/R-induced apoptosis, activation of Akt and GSK-3β, or oxidative stress. UB treatment enhanced mitochondrial biogenesis, and inhibition of mitochondrial fission using mdivi1 inhibited H/R-induced apoptosis. Ex vivo, UB treatment significantly decreased infarct size and improved functional recovery of the heart following global I/R. Activation of caspase-9, a key player of the mitochondrial death pathway, was significantly lower in UB-treated hearts post-I/R. UB, most likely acting via CXCR4, plays a protective role in H/R-induced myocyte apoptosis and myocardial I/R injury via modulation of mitochondrial homeostasis and the mitochondrial death pathway of apoptosis.

Indexed as

AnimalsApoptosisCardiovascular DiseasesCells, CulturedDisease Models, AnimalHypoxiaMaleMiceMice, Inbred C57BLMitochondria, HeartMyocytes, CardiacOxygenRatsRats, Sprague-DawleyReceptors, CXCR4UbiquitinCXCR4 protein, mouseCxcr4 protein, ratOxygenReceptors, CXCR4UbiquitinapoptoseapoptosiscœurCXCR4heartmyocytesubiquitinubiquitine

Identifiers

PMID31967865
PMCPMC7416794
OpenAlexW3002562631

What OpenQuestion holds

Textmetadata
LicenceTDM
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.