Evidence map›Paper›PMID 31820815›Full record

ReviewHistology and histopathology2020

The role of mitochondrial fusion and fission in the process of cardiac oxidative stress.

Fei Yu, Eltyeb Abdelwahid, Tao Xu, Longgang Hu, Man Wang, Yuzhen Li, Bassam Felipe Mogharbel, Katherine Athayde Teixeira de Carvalho, Luiz Cesar Guarita-Souza, Yi An and 1 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Histology and histopathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Mitochondrial Fusion and Fission in Neuronal Death Induced by Cerebral Ischemia-Reperfusion and Its Clinical Application: A Mini-Review.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Review
  6. Article
  7. Review
  8. Article
  9. Article
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

11 authors at 2 institutions in 1 country.

Fei YuInstitute for Translation Medicine, Medical College, Qingdao University, Qingdao, China.
Eltyeb AbdelwahidFeinberg School of Medicine, Feinberg Cardiovascular Research Institute, Northwestern University, Chicago, IL, USA. eltyeb.abdelwahid@northwestern.edu.
Tao XuInstitute for Translation Medicine, Medical College, Qingdao University, Qingdao, China.
Longgang HuDepartment of Cardiology, Affiliated Hospital of Qingdao University, Qingdao, China.
Man WangInstitute for Translation Medicine, Medical College, Qingdao University, Qingdao, China.
Yuzhen LiDepartment of Pathophysiology, Institute of Basic Medical Science, PLA General Hospital, Beijing, China.
Bassam Felipe MogharbelCell Therapy and Biotechnology in Regenerative Medicine Research Group, Pequeno Príncipe Faculty, Pelé Pequeno Príncipe Institute, Curitiba, Brazil.
Katherine Athayde Teixeira de CarvalhoCell Therapy and Biotechnology in Regenerative Medicine Research Group, Pequeno Príncipe Faculty, Pelé Pequeno Príncipe Institute, Curitiba, Brazil.
Luiz Cesar Guarita-SouzaExperimental Laboratory of Institute of Biological and Health Sciences of Pontifical Catholic University of Parana, Curitiba, Brazil.
Yi AnDepartment of cardiology, Affiliated hospital of Qingdao University, Qingdao, China. any2018@qdu.edu.cn.
Peifeng LiInstitute for Translation Medicine, Medical College, Qingdao University, Qingdao, China. peifli@qdu.edu.cn.
Institute of Basic Medical Sciences of the Chinese Academy of Medical SciencesQingdao University · CN

Funding

Applied Basic Research Programs of Qingdao, China 17-1-1-41-jchInnovative Talent Program of Qingdao City, China 18-1-2-6-zhcMajor Research Program of the National Natural Science Foundation of China 91849209National Science Foundation of Shandong Province, China ZR2017BEM025
6 · The paper itself

Abstract

Mitochondria are the energy suppliers in the cell and undergo constant fusion and fission to meet metabolic demand during the cell life cycle. Well-balanced mitochondrial dynamics are extremely important and necessary for cell survival as well as for tissue homeostasis. Cardiomyocytes contain large numbers of mitochondria to satisfy the high energy demand. It has been established that deregulated processes of mitochondrial dynamics play a major role in myocardial cell death. Currently, cardiac mitochondrial cell death pathways attract great attention in the cell biology and regenerative medicine fields. Importantly, mitochondrial dynamics are tightly linked to oxidative stress-induced cardiac damage. This review summarizes molecular mechanisms of mitochondrial fusion and fission processes and their potential roles in myocardial cell death triggered by oxidative stress. Advances in understanding the effect of both normal and abnormal mitochondrial dynamics on heart protection will lead to significant improvement of therapeutic discoveries.

Indexed as

Oxidative StressAnimalsCell DeathHumansMitochondriaMitochondrial DynamicsMyocytes, Cardiac

Identifiers

PMID31820815
OpenAlexW2997967244

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.