Evidence map›Paper›PMID 26537557›Full record

ReviewThe Journal of physiology2016

Mitochondrial dynamics, mitophagy and cardiovascular disease.

César Vásquez-Trincado, Ivonne García-Carvajal, Christian Pennanen, Valentina Parra, Joseph A Hill, Beverly A Rothermel, Sergio Lavandero

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 378 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
378citing papers in PubMed, 2 pooled it
11.6field-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

378 citing papers in PubMed, 2 syntheses or guidelines pooled it, 613 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
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  5. Article
  6. Article
  7. Review
  8. Therapeutic Lithium Enhances Klotho Expression and Mitochondrial Size and Branching in Human Cardiac Fibroblasts Involving Nuclear Factor-kappa B Inhibition.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026
    Article
  9. Article
  10. Article
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  14. ELABELA Targets Mitochondria to Modulate Heart Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  16. Article
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  18. Article
  19. Review
  20. Article

318 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

7 authors at 2 institutions in 2 countries.

César Vásquez-TrincadoAdvanced Centre for Chronic Disease (ACCDiS), Facultad Ciencias Quimicas y Farmaceuticas & Facultad Medicina, Universidad de Chile, Santiago, Chile.
Ivonne García-CarvajalAdvanced Centre for Chronic Disease (ACCDiS), Facultad Ciencias Quimicas y Farmaceuticas & Facultad Medicina, Universidad de Chile, Santiago, Chile.
Christian PennanenAdvanced Centre for Chronic Disease (ACCDiS), Facultad Ciencias Quimicas y Farmaceuticas & Facultad Medicina, Universidad de Chile, Santiago, Chile.
Valentina ParraAdvanced Centre for Chronic Disease (ACCDiS), Facultad Ciencias Quimicas y Farmaceuticas & Facultad Medicina, Universidad de Chile, Santiago, Chile.
Joseph A HillDepartment of Internal Medicine (Cardiology Division), University of Texas Southwestern Medical Centre, Dallas, TX, USA.
Beverly A RothermelDepartment of Internal Medicine (Cardiology Division), University of Texas Southwestern Medical Centre, Dallas, TX, USA.
Sergio LavanderoAdvanced Centre for Chronic Disease (ACCDiS), Facultad Ciencias Quimicas y Farmaceuticas & Facultad Medicina, Universidad de Chile, Santiago, Chile.
Advanced Center for Chronic Diseases · CLThe University of Texas Southwestern Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac hypertrophy is often initiated as an adaptive response to haemodynamic stress or myocardial injury, and allows the heart to meet an increased demand for oxygen. Although initially beneficial, hypertrophy can ultimately contribute to the progression of cardiac disease, leading to an increase in interstitial fibrosis and a decrease in ventricular function. Metabolic changes have emerged as key mechanisms involved in the development and progression of pathological remodelling. As the myocardium is a highly oxidative tissue, mitochondria play a central role in maintaining optimal performance of the heart. 'Mitochondrial dynamics', the processes of mitochondrial fusion, fission, biogenesis and mitophagy that determine mitochondrial morphology, quality and abundance have recently been implicated in cardiovascular disease. Studies link mitochondrial dynamics to the balance between energy demand and nutrient supply, suggesting that changes in mitochondrial morphology may act as a mechanism for bioenergetic adaptation during cardiac pathological remodelling. Another critical function of mitochondrial dynamics is the removal of damaged and dysfunctional mitochondria through mitophagy, which is dependent on the fission/fusion cycle. In this article, we discuss the latest findings regarding the impact of mitochondrial dynamics and mitophagy on the development and progression of cardiovascular pathologies, including diabetic cardiomyopathy, atherosclerosis, damage from ischaemia-reperfusion, cardiac hypertrophy and decompensated heart failure. We will address the ability of mitochondrial fusion and fission to impact all cell types within the myocardium, including cardiac myocytes, cardiac fibroblasts and vascular smooth muscle cells. Finally, we will discuss how these findings can be applied to improve the treatment and prevention of cardiovascular diseases.

Indexed as

AnimalsAutophagyCardiovascular DiseasesHumansMitochondriaMitochondrial Dynamics

Identifiers

PMID26537557
PMCPMC5341713
OpenAlexW1926228770

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.