Evidence map›Paper›PMID 35523864›Full record

ReviewNature reviews. Cardiology2022

The role of mitochondrial fission in cardiovascular health and disease.

Justin M Quiles, Åsa B Gustafsson

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cardiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed, 1 pooled it
22.5field-weighted citation impact, top 1% 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

162 citing papers in PubMed, 1 synthesis or guideline pooled it, 272 citations in OpenAlex.

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102 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Justin M QuilesSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, CA, USA.
Åsa B GustafssonSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, CA, USA. abgustafsson@ucsd.edu.ORCID 0000-0001-6347-8210
University of California San Diego · US

Funding

Secretion of mitochondria as a cellular quality control mechanismR01HL155281 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUSTAFSSON, ASA B. · 2021 to 2024
$2.3M
Autophagy and Megamitochondria in Cardiac Aging and Heart FailureR01HL157265 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUSTAFSSON, ASA B. · 2021 to 2024
$1.9M
MCL-1 is a critical regulator of mitochondrial dynamics and function in myocytesR01HL132300 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUSTAFSSON, ASA B. · 2017 to 2020
$1.7M
Role of the Endosomal-Lysosomal Pathway in Mitochondrial Quality ControlR01HL138560 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUSTAFSSON, ASA B. · 2017 to 2020
$1.6M
NHLBI NIH HHS R01 HL132300NHLBI NIH HHS R01 HL138560NHLBI NIH HHS R01HL138560NHLBI NIH HHS R01 HL155281NHLBI NIH HHS R01HL155281NHLBI NIH HHS R01 HL157265
6 · The paper itself

Abstract

Mitochondria are organelles involved in the regulation of various important cellular processes, ranging from ATP generation to immune activation. A healthy mitochondrial network is essential for cardiovascular function and adaptation to pathological stressors. Mitochondria undergo fission or fusion in response to various environmental cues, and these dynamic changes are vital for mitochondrial function and health. In particular, mitochondrial fission is closely coordinated with the cell cycle and is linked to changes in mitochondrial respiration and membrane permeability. Another key function of fission is the segregation of damaged mitochondrial components for degradation by mitochondrial autophagy (mitophagy). Mitochondrial fission is induced by the large GTPase dynamin-related protein 1 (DRP1) and is subject to sophisticated regulation. Activation requires various post-translational modifications of DRP1, actin polymerization and the involvement of other organelles such as the endoplasmic reticulum, Golgi apparatus and lysosomes. A decrease in mitochondrial fusion can also shift the balance towards mitochondrial fission. Although mitochondrial fission is necessary for cellular homeostasis, this process is often aberrantly activated in cardiovascular disease. Indeed, strong evidence exists that abnormal mitochondrial fission directly contributes to disease development. In this Review, we compare the physiological and pathophysiological roles of mitochondrial fission and discuss the therapeutic potential of preventing excessive mitochondrial fission in the heart and vasculature.

Indexed as

ActinsMitochondrial DynamicsAdenosine TriphosphateDynaminsGTP PhosphohydrolasesHumansActinsAdenosine TriphosphateDynaminsGTP Phosphohydrolases

Identifiers

PMID35523864
PMCPMC10584015
OpenAlexW4229021244

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.