Evidence map›Paper›PMID 31366990›Full record

ArticleCell research2019

NDUFAB1 confers cardio-protection by enhancing mitochondrial bioenergetics through coordination of respiratory complex and supercomplex assembly.

Tingting Hou, Rufeng Zhang, Chongshu Jian, Wanqiu Ding, Yanru Wang, Shukuan Ling, Qi Ma, Xinli Hu, Heping Cheng, Xianhua Wang

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Cell research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05202938 (Energy MEtabolism of Septic Heart.), which is not on this map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.1field-weighted citation impact, top 5% 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.

NCT05202938 unknown statusnot on this mapstarted 2022, after this paper: background citation

Energy MEtabolism of Septic Heart.

TypeobservationalSponsorCentre de recherche du Centre hospitalier universitaire de SherbrookeRan2022 to 2024Enrolled32ConditionsSeptic Shock, Chronic Heart FailureArmsultrasound cardiography, FDG PET scan, Palmitate PET scan, Acetate PET scan, Blood sampling
3 · Its place in the literature

Who cites it

67 citing papers in PubMed, 111 citations in OpenAlex.

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  15. A hydrophobic photouncaging reaction to profile the lipid droplet interactome in tissues.Proceedings of the National Academy of Sciences of the United States of America · 2025
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7 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

10 authors at 3 institutions in 1 country.

Tingting HouState Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing, 100871, China.
Rufeng ZhangState Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing, 100871, China.
Chongshu JianState Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing, 100871, China.
Wanqiu DingState Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing, 100871, China.
Yanru WangState Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing, 100871, China.
Shukuan LingState Key Laboratory of Space Medicine Fundamentals and Application, China Astronaut Research and Training Center, Beijing, 100094, China.
Qi MaState Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing, 100871, China.
Xinli HuState Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing, 100871, China.
Heping ChengState Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing, 100871, China. chengp@pku.edu.cn.
Xianhua WangState Key Laboratory of Membrane Biology, Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing, 100871, China. xianhua@pku.edu.cn.
Center for Life Sciences · CNPeking University · CNChina Astronaut Research and Training Center · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31470811National Natural Science Foundation of China (National Science Foundation of China) 31521062National Natural Science Foundation of China (National Science Foundation of China) 31670039
6 · The paper itself

Abstract

The impairment of mitochondrial bioenergetics, often coupled with exaggerated reactive oxygen species (ROS) production, is a fundamental disease mechanism in organs with a high demand for energy, including the heart. Building a more robust and safer cellular powerhouse holds the promise for protecting these organs in stressful conditions. Here, we demonstrate that NADH:ubiquinone oxidoreductase subunit AB1 (NDUFAB1), also known as mitochondrial acyl carrier protein, acts as a powerful cardio-protector by conferring greater capacity and efficiency of mitochondrial energy metabolism. In particular, NDUFAB1 not only serves as a complex I subunit, but also coordinates the assembly of respiratory complexes I, II, and III, and supercomplexes, through regulating iron-sulfur biosynthesis and complex I subunit stability. Cardiac-specific deletion of Ndufab1 in mice caused defective bioenergetics and elevated ROS levels, leading to progressive dilated cardiomyopathy and eventual heart failure and sudden death. Overexpression of Ndufab1 effectively enhanced mitochondrial bioenergetics while limiting ROS production and protected the heart against ischemia-reperfusion injury. Together, our findings identify that NDUFAB1 is a crucial regulator of mitochondrial energy and ROS metabolism through coordinating the assembly of respiratory complexes and supercomplexes, and thus provide a potential therapeutic target for the prevention and treatment of heart failure.

Indexed as

Energy MetabolismAnimalsCardiomyopathy, DilatedElectron Transport Complex IHeart FailureMaleMembrane Potential, MitochondrialMiceMice, KnockoutMitochondriaMyocardiumMyocytes, CardiacRatsRats, Sprague-DawleyReactive Oxygen SpeciesRNA InterferenceElectron Transport Complex IReactive Oxygen SpeciesRNA, Small Interfering

Identifiers

PMID31366990
PMCPMC6796901
OpenAlexW2966377165

What OpenQuestion holds

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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.