Evidence map›Paper›PMID 37237146›Full record

ReviewNature reviews. Cardiology2023

Metabolic mechanisms in physiological and pathological cardiac hypertrophy: new paradigms and challenges.

Julia Ritterhoff, Rong Tian

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed
25.3field-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

141 citing papers in PubMed, 194 citations in OpenAlex.

  1. Article
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  11. USP11 alleviates pathological cardiac hypertrophy via stabilizing SIRT6.Cellular and molecular life sciences : CMLS · 2026
    Article
  12. Article
  13. Review
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81 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 2 countries.

Julia RitterhoffMolecular and Translational Cardiology, Department of Internal Medicine III, Heidelberg University Hospital, Heidelberg, Germany. julia.ritterhoff@uni-heidelberg.de.ORCID 0000-0002-3419-4830
Rong TianMitochondria and Metabolism Center, Department of Anaesthesiology and Pain Medicine, University of Washington, Seattle, WA, USA. rongtian@uw.edu.ORCID 0000-0002-3676-3830
University of Washington · US

Funding

NAD+/NADH ratio, protein acetylation and mitochondrial functionR01HL110349 · NHLBI · UNIVERSITY OF WASHINGTON · PI TIAN, RONG · 2011 to 2020
$5.7M
Mechanistic Studies of NAD+/NADH in Human Heart FailureR01HL144937 · NHLBI · UNIVERSITY OF WASHINGTON · PI O'BRIEN, KEVIN D., TIAN, RONG · 2019 to 2023
$4.2M
Mitochondrial metabolism and macrophage function post MIR01HL149695 · NHLBI · UNIVERSITY OF WASHINGTON · PI TIAN, RONG · 2020 to 2023
$2.9M
The heart failure interactomeR01HL144778 · NHLBI · UNIVERSITY OF WASHINGTON · PI BRUCE, JAMES EDWARD · 2019 to 2022
$2.7M
Mitochondrial function and glycolytic switch in pathological cardiac hypertrophyR01HL142628 · NHLBI · UNIVERSITY OF WASHINGTON · PI TIAN, RONG · 2018 to 2021
$2.4M
NHLBI NIH HHS R01 HL110349NHLBI NIH HHS R01 HL142628NHLBI NIH HHS R01 HL144778NHLBI NIH HHS R01 HL144937NHLBI NIH HHS R01 HL149695
6 · The paper itself

Abstract

Cardiac metabolism is vital for heart function. Given that cardiac contraction requires a continuous supply of ATP in large quantities, the role of fuel metabolism in the heart has been mostly considered from the perspective of energy production. However, the consequence of metabolic remodelling in the failing heart is not limited to a compromised energy supply. The rewired metabolic network generates metabolites that can directly regulate signalling cascades, protein function, gene transcription and epigenetic modifications, thereby affecting the overall stress response of the heart. In addition, metabolic changes in both cardiomyocytes and non-cardiomyocytes contribute to the development of cardiac pathologies. In this Review, we first summarize how energy metabolism is altered in cardiac hypertrophy and heart failure of different aetiologies, followed by a discussion of emerging concepts in cardiac metabolic remodelling, that is, the non-energy-generating function of metabolism. We highlight challenges and open questions in these areas and finish with a brief perspective on how mechanistic research can be translated into therapies for heart failure.

Indexed as

CardiomegalyHeart FailureEnergy MetabolismHumansMyocardiumMyocytes, CardiacSignal Transduction

Identifiers

PMID37237146
OpenAlexW4378417031

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.