Evidence map›Paper›PMID 35958686›Full record

ReviewJACC. Basic to translational science2022

Short-Chain Carbon Sources: Exploiting Pleiotropic Effects for Heart Failure Therapy.

Azariyas A Challa, E Douglas Lewandowski

Open access · goldAbstract readReview
In one paragraph

Review in JACC. Basic to translational science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. MDH2 S246 phosphorylation protects mitochondria against hypoxia/reoxygenation injury due to acetate/lactate metabolism.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Article
  5. Review
  6. Metabolic syndrome and a broken heart: trust your gut or risk your heart.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  7. Review
  8. Review
  9. Review
  10. The impact of lipid metabolism on ferroptosis in myocardial ischemia-reperfusion injury.Apoptosis : an international journal on programmed cell death · 2025
    Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Metabolic flux in the driver's seat during cardiac health and disease.Journal of molecular and cellular cardiology · 2023
    Review
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.

Azariyas A ChallaDivision of Cardiovascular Medicine, The Ohio State University College of Medicine, Columbus, Ohio, USA.
E Douglas LewandowskiDivision of Cardiovascular Medicine, The Ohio State University College of Medicine, Columbus, Ohio, USA.
The Ohio State University · US

Funding

Magnetic Resonance of Cardiac C13 Flux & Metabolism RateR01HL049244 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LEWANDOWSKI, E DOUGLAS · 1993 to 2018
$3.7M
Maladaptive Expression of Metabolic Enzymes and Activity in Heart FailureR01HL132525 · NHLBI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI LEWANDOWSKI, E DOUGLAS · 2016 to 2019
$2.5M
Postdoctoral Training in Cardiometabolic ScienceT32HL149637 · NHLBI · OHIO STATE UNIVERSITY · PI HSUEH, WILLA A, SMITH, SAKIMA AHMAD · 2020 to 2024
$1.5M
NHLBI NIH HHS R01 HL049244NHLBI NIH HHS R01 HL132525NHLBI NIH HHS T32 HL149637
6 · The paper itself

Abstract

Heart failure (HF) remains the leading cause of morbidity and mortality in the developed world, highlighting the urgent need for novel, effective therapeutics. Recent studies support the proposition that improved myocardial energetics as a result of ketone body (KB) oxidation may account for the intriguing beneficial effects of sodium-glucose cotransporter-2 inhibitors in patients with HF. Similar small molecules, short-chain fatty acids (SCFAs) are now realized to be preferentially oxidized over KBs in failing hearts, contradicting the notion of KBs as a rescue "superfuel." In addition to KBs and SCFAs being alternative fuels, both exert a wide array of nonmetabolic functions, including molecular signaling and epigenetics and as effectors of inflammation and immunity, blood pressure regulation, and oxidative stress. In this review, the authors present a perspective supported by new evidence that the metabolic and unique nonmetabolic activities of KBs and SCFAs hold promise for treatment of patients with HF with reduced ejection fraction and those with HF with preserved ejection fraction.

Indexed as

BP, blood pressureCoA, coenzyme ACPT1, carnitine palmitoyltransferase IFFAR, free fatty acid receptorGPR, G protein–coupled receptorheart failureHF, heart failureHFpEFHFpEF, heart failure with preserved ejection fractionHFrEFKB, ketone bodyketonesLCFA, long-chain fatty acidSCFA, short-chain fatty acidSGLT2, sodium-glucose cotransporter-2short-chain fatty acidsβ-HB, β-hydroxybutyrate

Identifiers

PMID35958686
PMCPMC9357564
OpenAlexW4220740254

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.