Evidence map›Paper›PMID 28918113›Full record

ReviewBiochimica et biophysica acta. Molecular basis of disease2018

Regulation of mitochondrial bioenergetics by the non-canonical roles of mitochondrial dynamics proteins in the heart.

Wang Wang, Celia Fernandez-Sanz, Shey-Shing Sheu

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta. Molecular basis of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Neurohormonal connections with mitochondria in cardiomyopathy and other diseases.American journal of physiology. Cell physiology · 2022
    Review
  14. Article
  15. Review
  16. Review
  17. The role of Drp1 in mitophagy and cell death in the heart.Journal of molecular and cellular cardiology · 2020
    Review
  18. Why don't mice lacking the mitochondrial CaThe Journal of physiology · 2020
    Review
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

Wang WangMitochondria and Metabolism Center, Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA 98109, USA. Electronic address: wangwang@u.washington.edu.
Celia Fernandez-SanzCenter for Translational Medicine, Department of Medicine, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Shey-Shing SheuCenter for Translational Medicine, Department of Medicine, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA 19107, USA. Electronic address: Shey-Shing.Sheu@jefferson.edu.
Thomas Jefferson University · USUniversity of Washington · US

Funding

Ca2+ and ROS Crosstalk Signaling in Cardiac MitochondriaR01HL093671 · NHLBI · UNIVERSITY OF ROCHESTER · PI SHEU, SHEY-SHING · 2010 to 2023
$5.1M
Mitochondria-SR Tethering: Its Role in Cardiac Bioenergetics and Ca2+ DynamicsR01HL122124 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI CSORDAS, GYORGY, SHEU, SHEY-SHING · 2014 to 2025
$4.0M
Dynamin-Related Protein Drp1 Regulates Cardiac Excitation-Contraction-Bioenergetics CouplingR01HL137266 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI SHEU, SHEY-SHING, WANG, WANG · 2018 to 2021
$2.5M
Mitochondrial Respiration and Superoxide Production in Healthy and Failing HeartR01HL114760 · NHLBI · UNIVERSITY OF WASHINGTON · PI WANG, WANG · 2012 to 2016
$2.1M
Vevo 2100 ultrasound scannerS10OD010408 · OD · THOMAS JEFFERSON UNIVERSITY · PI FORSBERG, FLEMMING · 2012 to 2012
$525k
NHLBI NIH HHS R01 HL093671NHLBI NIH HHS R01 HL114760NHLBI NIH HHS R01 HL122124NHLBI NIH HHS R01 HL137266NIH HHS S10 OD010408
6 · The paper itself

Abstract

Recent advancement in mitochondrial research has significantly extended our knowledge on the role and regulation of mitochondria in health and disease. One important breakthrough is the delineation of how mitochondrial morphological changes, termed mitochondrial dynamics, are coupled to the bioenergetics and signaling functions of mitochondria. In general, it is believed that fusion leads to an increased mitochondrial respiration efficiency and resistance to stress-induced dysfunction while fission does the contrary. This concept seems not applicable to adult cardiomyocytes. The mitochondria in adult cardiomyocytes exhibit fragmented morphology (tilted towards fission) and show less networking and movement as compared to other cell types. However, being the most energy-demanding cells, cardiomyocytes in the adult heart possess vast number of mitochondria, high level of energy flow, and abundant mitochondrial dynamics proteins. This apparent discrepancy could be explained by recently identified new functions of the mitochondrial dynamics proteins. These "non-canonical" roles of mitochondrial dynamics proteins range from controlling inter-organelle communication to regulating cell viability and survival under metabolic stresses. Here, we summarize the newly identified non-canonical roles of mitochondrial dynamics proteins. We focus on how these fission and fusion independent roles of dynamics proteins regulate mitochondrial bioenergetics. We also discuss potential molecular mechanisms, unique intracellular location, and the cardiovascular disease relevance of these non-canonical roles of the dynamics proteins. We propose that future studies are warranted to differentiate the canonical and non-canonical roles of dynamics proteins and to identify new approaches for the treatment of heart diseases. This article is part of a Special issue entitled Cardiac adaptations to obesity, diabetes and insulin resistance, edited by Professors Jan F.C. Glatz, Jason R.B. Dyck and Christine Des Rosiers.

Indexed as

Energy MetabolismMitochondrial DynamicsHeart DiseasesHumansMitochondria, HeartMitochondrial ProteinsMyocytes, CardiacSignal TransductionMitochondrial ProteinsCardiac bioenergeticsMetabolic heart diseaseMitochondria associated membranesMitochondrial dynamics proteins

Identifiers

PMID28918113
PMCPMC5851799
OpenAlexW2756352838

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.