Evidence map›Paper›PMID 30124471›Full record

ReviewThe Journal of clinical investigation2018

Mitochondrial dysfunction in pathophysiology of heart failure.

Bo Zhou, Rong Tian

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05593055 (Mineralocorticoid Receptor, Coronary Microvascular Function, and Cardiac Efficiency in Hypertension), which is not on this map. Cited by 580 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
580citing papers in PubMed, 2 pooled it
19.8field-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.

NCT05593055 phase4recruitingnot on this mapstarted 2023, after this paper: background citation

Mineralocorticoid Receptor, Coronary Microvascular Function, and Cardiac Efficiency in Hypertension

TypeinterventionalSponsorBrigham and Women's HospitalRan2023 to 2027Enrolled75ConditionsHypertension, Left Ventricular HypertrophyArmsEplerenone, Chlorthalidone, Potassium
3 · Its place in the literature

Who cites it

580 citing papers in PubMed, 2 syntheses or guidelines pooled it, 883 citations in OpenAlex.

  1. Pooled it
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  10. 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
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520 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.

Bo Zhou
Rong Tian
University of Washington · US

Funding

Engineered Stem Cells for Cardiac RepairR01HL128368 · NHLBI · UNIVERSITY OF WASHINGTON · PI REGNIER, MICHAEL · 2018 to 2025
$6.1M
NAD+/NADH ratio, protein acetylation and mitochondrial functionR01HL110349 · NHLBI · UNIVERSITY OF WASHINGTON · PI TIAN, RONG · 2011 to 2020
$5.7M
Glucose And BCAA Metabolism in the HeartR01HL118989 · NHLBI · UNIVERSITY OF WASHINGTON · PI TIAN, RONG · 2014 to 2017
$3.1M
Fatty acid oxidation suppresses cardiac hypertrophyR01HL129510 · NHLBI · UNIVERSITY OF WASHINGTON · PI TIAN, RONG · 2015 to 2018
$2.8M
Mitochondrial function and glycolytic switch in pathological cardiac hypertrophyR01HL142628 · NHLBI · UNIVERSITY OF WASHINGTON · PI TIAN, RONG · 2018 to 2021
$2.4M
Safety and Tolerability of the Nutritional Supplement, Nicotinamide Riboside, in Systolic Heart FailureR21HL126209 · NHLBI · UNIVERSITY OF WASHINGTON · PI O'BRIEN, KEVIN D., TIAN, RONG · 2015 to 2017
$541k
NHLBI NIH HHS R01 HL110349NHLBI NIH HHS R01 HL118989NHLBI NIH HHS R01 HL128368NHLBI NIH HHS R01 HL129510NHLBI NIH HHS R01 HL142628NHLBI NIH HHS R21 HL126209
6 · The paper itself

Abstract

Mitochondrial dysfunction has been implicated in the development of heart failure. Oxidative metabolism in mitochondria is the main energy source of the heart, and the inability to generate and transfer energy has long been considered the primary mechanism linking mitochondrial dysfunction and contractile failure. However, the role of mitochondria in heart failure is now increasingly recognized to be beyond that of a failed power plant. In this Review, we summarize recent evidence demonstrating vicious cycles of pathophysiological mechanisms during the pathological remodeling of the heart that drive mitochondrial contributions from being compensatory to being a suicide mission. These mechanisms include bottlenecks of metabolic flux, redox imbalance, protein modification, ROS-induced ROS generation, impaired mitochondrial Ca2+ homeostasis, and inflammation. The interpretation of these findings will lead us to novel avenues for disease mechanisms and therapy.

Indexed as

Adenosine TriphosphateAnimalsCalciumDisease ProgressionEnergy MetabolismHeart FailureHumansInflammationMitochondria, HeartModels, CardiovascularOxidation-ReductionOxidative StressReactive Oxygen SpeciesAdenosine TriphosphateCalciumReactive Oxygen Species

Identifiers

PMID30124471
PMCPMC6118589
OpenAlexW2885025259

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.