Evidence map›Paper›PMID 37392421›Full record

ReviewCardiovascular research2023

Cardiac lipid metabolism, mitochondrial function, and heart failure.

Lorenzo Da Dalt, Ainara G Cabodevilla, Ira J Goldberg, Giuseppe Danilo Norata

Open access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
163citing papers in PubMed, 2 pooled it
34.5field-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

163 citing papers in PubMed, 2 syntheses or guidelines pooled it, 188 citations in OpenAlex.

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103 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

4 authors at 2 institutions in 2 countries.

Lorenzo Da DaltDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Via Balzaretti 9, Milan, Italy.ORCID 0000-0002-6298-8689
Ainara G CabodevillaDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, New York University Grossman School of Medicine, 550 1st Ave., New York, NY, USA.ORCID 0000-0002-4026-7637
Ira J GoldbergDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, New York University Grossman School of Medicine, 550 1st Ave., New York, NY, USA.
Giuseppe Danilo NorataDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Via Balzaretti 9, Milan, Italy.ORCID 0000-0002-6081-1257
New York University · USUniversity of Milan · IT

Funding

Translational Research CoreP30DK020541 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI JEFFREY E. PESSIN · 2015 to 2026
$27.7M
NIDDK NIH HHS P30 DK020541
6 · The paper itself

Abstract

A fine balance between uptake, storage, and the use of high energy fuels, like lipids, is crucial in the homeostasis of different metabolic tissues. Nowhere is this balance more important and more precarious than in the heart. This highly energy-demanding muscle normally oxidizes almost all the available substrates to generate energy, with fatty acids being the preferred source under physiological conditions. In patients with cardiomyopathies and heart failure, changes in the main energetic substrate are observed; these hearts often prefer to utilize glucose rather than oxidizing fatty acids. An imbalance between uptake and oxidation of fatty acid can result in cellular lipid accumulation and cytotoxicity. In this review, we will focus on the sources and uptake pathways used to direct fatty acids to cardiomyocytes. We will then discuss the intracellular machinery used to either store or oxidize these lipids and explain how disruptions in homeostasis can lead to mitochondrial dysfunction and heart failure. Moreover, we will also discuss the role of cholesterol accumulation in cardiomyocytes. Our discussion will attempt to weave in vitro experiments and in vivo data from mice and humans and use several human diseases to illustrate metabolism gone haywire as a cause of or accomplice to cardiac dysfunction.

Indexed as

Heart FailureMyocardiumAnimalsEnergy MetabolismFatty AcidsHeartHumansLipid MetabolismMiceMitochondriaMyocytes, CardiacOxidation-ReductionFatty AcidsCholesterolHeart failureLipidsLipoprotein

Identifiers

PMID37392421
PMCPMC10681665
OpenAlexW4382765961

What Socratic 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 Socratic graph.