Evidence map›Paper›PMID 21502372›Full record

ReviewCardiovascular research2011

Branched-chain amino acid metabolism in heart disease: an epiphenomenon or a real culprit?

Ying Huang, Meiyi Zhou, Haipeng Sun, Yibin Wang

2 registry-linked trialsOpen access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
2.4field-weighted citation impact, top 11% 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.

NCT02894931 naunknown statusnot on this mapstarted 2016, after this paper: background citation

Effects of Dietary Interventions (Sugars, Amino Acids and Artificial Sweeteners) on Serum and Macrophage Atherogenicity

TypeinterventionalSponsorRambam Health Care CampusRan2016 to 2018Enrolled90ConditionsDietary Habits, Serum, Disease, Macrophage AtherogenicityArmsmonosaccharides, Disaccharides, Amino acids, Artificial Sweeteners, Control- water
NCT03180775 naunknown statusnot on this mapstarted 2017, after this paper: background citation

Effects of Dietary Amino Acids on Serum and Macrophage Atherogenicity

TypeinterventionalSponsorRambam Health Care CampusRan2017 to 2018Enrolled110ConditionsAtherosclerosis, Diet Modification, Serum, DiseaseArmsCellulose (control), Glycine, Alanine, Leucine, Isoleucine
3 · Its place in the literature

Who cites it

114 citing papers in PubMed, 207 citations in OpenAlex.

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  19. Cardiac Metabolism, Reprogramming, and Diseases.Journal of cardiovascular translational research · 2024
    Review
  20. Review

54 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 1 institution in 1 country.

Ying HuangDepartment of Pathophysiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Meiyi Zhou
Haipeng Sun
Yibin Wang
Shanghai Jiao Tong University · CN

Funding

ROLE OF P38 MAPK AND PP2C IN ISCHEMIC INJURY AND PROTECTIONP01HL080111 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WEISS, JAMES N · 2005 to 2009
$11.6M
Revealing Cardiovascular Stress Regulation beyond the Diffraction LimitR01HL088640 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI STEFANI, ENRICO · 2007 to 2011
$5.3M
Novel Signaling Mechanisms and Molecular Targets in the Stressed MyocardiumR01HL098954 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PING, PEIPEI, WANG, YIBIN · 2010 to 2013
$3.0M
Novel Function and Regulatory Mechanisms of Stress Kinase p38 in HeartR01HL103205 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WANG, YIBIN · 2010 to 2014
$1.9M
NHLBI NIH HHS HL080111NHLBI NIH HHS HL088640NHLBI NIH HHS HL098954NHLBI NIH HHS HL103205NHLBI NIH HHS HL70079
6 · The paper itself

Abstract

Metabolic remodelling is an integral part of the pathogenesis of heart failure. Although much progress has been made in our current understanding of the metabolic impairment involving carbohydrates and fatty acids in failing hearts, relatively little is known about the changes and potential impact of amino acid metabolism in the onset of heart diseases. Although most amino acid catabolic activities are found in the liver, branched-chain amino acid (BCAA) catabolism requires activity in several non-hepatic tissues, including cardiac muscle, diaphragm, brain and kidney. In this review, the new insights into the regulation of cardiac BCAA catabolism and functional impact on cardiac development and physiology will be discussed along with the potential contribution of impairment in BCAA catabolism to heart diseases. A particular focus will be the new information obtained from recently developed genetic models with BCAA catabolic defects and metabolomic studies in human and animal models. These studies have revealed the potential role of BCAA catabolism in cardiac pathophysiology and have helped to distinguish BCAA metabolic defects as an under-appreciated culprit in cardiac diseases rather than an epiphenomenon associated with metabolic remodelling in the failing heart.

Indexed as

Amino Acids, Branched-ChainAnimalsEnergy MetabolismHeart FailureHumansPhosphoprotein PhosphatasesProtein Phosphatase 2CVentricular RemodelingAmino Acids, Branched-ChainPhosphoprotein PhosphatasesProtein Phosphatase 2C

Identifiers

PMID21502372
PMCPMC3078803
OpenAlexW2167039546

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.