Evidence map›Paper›PMID 30177752›Full record

ReviewNature reviews. Cardiology2019

Targeting mitochondria for cardiovascular disorders: therapeutic potential and obstacles.

Massimo Bonora, Mariusz R Wieckowski, David A Sinclair, Guido Kroemer, Paolo Pinton, Lorenzo Galluzzi

Abstract readReview
In one paragraph

Review in Nature reviews. Cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

149 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  11. Mitophagy in cardiovascular diseases: a literature review.Cardiovascular diagnosis and therapy · 2026
    Review
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89 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

6 authors.

Massimo BonoraRuth L. and David S. Gottesman Institute for Stem Cell, Regenerative Medicine Research, Department of Cell Biology and Stem Cell Institute, Albert Einstein College of Medicine, Bronx, NY, USA.
Mariusz R WieckowskiDepartment of Biochemistry, Nencki Institute of Experimental Biology, Warsaw, Poland.
David A SinclairDepartment of Genetics, Paul F. Glenn Center for the Biology of Aging, Harvard Medical School, Boston, MA, USA.
Guido KroemerEquipe 11 labellisée Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France.
Paolo PintonDepartment of Morphology, Surgery, and Experimental Medicine, Section of Pathology, Oncology, and Experimental Biology, Laboratory for Technologies of Advanced Therapies, University of Ferrara, Ferrara, Italy. pnp@unife.it.
Lorenzo GalluzziUniversité Paris Descartes/Paris V, Paris, France. deadoc@vodafone.it.

Funding

Uncovering the Human SecretomeDP1AG058605 · NIA · HARVARD MEDICAL SCHOOL · PI SINCLAIR, DAVID A. · 2017 to 2021
$5.9M
Role of Sgs1 DNA helicase in telomere maintenanceR01AG019719 · NIA · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI SINCLAIR, DAVID A. · 2001 to 2022
$5.3M
SIRT1 as a regulator of health and lifespan of mammalsR37AG028730 · NIA · HARVARD MEDICAL SCHOOL · PI SINCLAIR, DAVID A. · 2012 to 2021
$4.1M
Elucidating mechanisms of SIRT1 activationR01DK100263 · NIDDK · HARVARD MEDICAL SCHOOL · PI SINCLAIR, DAVID A. · 2016 to 2020
$2.5M
SIRT as a regulator of health and lifespan of mammalsR01AG028730 · NIA · HARVARD MEDICAL SCHOOL · PI SINCLAIR, DAVID A. · 2007 to 2011
$1.7M
Nicotinamide Mononucleotide (NMN) as a Novel Therapeutic in the Treatment of Oral MucositisR21DE027490 · NIDCR · HARVARD MEDICAL SCHOOL · PI SINCLAIR, DAVID A. · 2018 to 2019
$466k
NIA NIH HHS DP1 AG058605NIA NIH HHS R01 AG019719NIA NIH HHS R01 AG028730NIA NIH HHS R37 AG028730NIDCR NIH HHS R21 DE027490NIDDK NIH HHS R01 DK100263
6 · The paper itself

Abstract

A large body of evidence indicates that mitochondrial dysfunction has a major role in the pathogenesis of multiple cardiovascular disorders. Over the past 2 decades, extraordinary efforts have been focused on the development of agents that specifically target mitochondria for the treatment of cardiovascular disease. Despite such an intensive wave of investigation, no drugs specifically conceived to modulate mitochondrial functions are currently available for the clinical management of cardiovascular disease. In this Review, we discuss the therapeutic potential of targeting mitochondria in patients with cardiovascular disease, examine the obstacles that have restrained the development of mitochondria-targeting agents thus far, and identify strategies that might empower the full clinical potential of this approach.

Indexed as

AnimalsCardiovascular AgentsCardiovascular DiseasesHumansMitochondria, HeartMolecular Targeted TherapyCardiovascular Agents

Identifiers

PMID30177752
PMCPMC6349394

What OpenQuestion holds

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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.