Evidence map›Paper›PMID 24614109›Full record

ArticleThe Journal of clinical investigation2014

Protein kinetic signatures of the remodeling heart following isoproterenol stimulation.

Maggie P Y Lam, Ding Wang, Edward Lau, David A Liem, Allen K Kim, Dominic C M Ng, Xiangbo Liang, Brian J Bleakley, Chenguang Liu, Jason D Tabaraki and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

63 citing papers in PubMed, 101 citations in OpenAlex.

  1. Trial
  2. Kinetic Lipidomics: QuantifyingbioRxiv : the preprint server for biology · 2026
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  11. Metabolomic and proteomic applications to exercise biomedicine.Translational exercise biomedicine · 2024
    Review
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  15. Article
  16. Review
  17. Review
  18. Article
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  20. Article

3 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

14 authors at 2 institutions in 2 countries.

Maggie P Y Lam
Ding Wang
Edward Lau
David A Liem
Allen K Kim
Dominic C M Ng
Xiangbo Liang
Brian J Bleakley
Chenguang Liu
Jason D Tabaraki
Martin Cadeiras
Yibin Wang
Mario C Deng
Peipei Ping
University of California, Los Angeles · USCzech Academy of Sciences, Institute of Physiology · CZ

Funding

Subcellular organization and Ca+2 signaling in heart failureP01HL070709 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI ROGERS, TERRY B. · 2002 to 2006
$7.1M
PKC epsilon and Src PTK Signaling in PreconditioningR37HL063901 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PING, PEIPEI · 2010 to 2016
$2.7M
Novel Mechanism of SR Calcium Regulation in Cardiac DysfunctionR01HL108186 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WANG, YIBIN · 2011 to 2015
$1.9M
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
Novel Regulatory Circuit in Cardiac Hypertrophy Via RNA SplicingR01HL122737 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WANG, YIBIN · 2014 to 2017
$1.5M
NHLBI NIH HHS HHSN268201000035CNHLBI NIH HHS HL-R37-63901NHLBI NIH HHS P01 HL070709NHLBI NIH HHS R01 HL103205NHLBI NIH HHS R01 HL108186NHLBI NIH HHS R01 HL122737
6 · The paper itself

Abstract

Protein temporal dynamics play a critical role in time-dimensional pathophysiological processes, including the gradual cardiac remodeling that occurs in early-stage heart failure. Methods for quantitative assessments of protein kinetics are lacking, and despite knowledge gained from single-protein studies, integrative views of the coordinated behavior of multiple proteins in cardiac remodeling are scarce. Here, we developed a workflow that integrates deuterium oxide (2H2O) labeling, high-resolution mass spectrometry (MS), and custom computational methods to systematically interrogate in vivo protein turnover. Using this workflow, we characterized the in vivo turnover kinetics of 2,964 proteins in a mouse model of β-adrenergic-induced cardiac remodeling. The data provided a quantitative and longitudinal view of cardiac remodeling at the molecular level, revealing widespread kinetic regulations in calcium signaling, metabolism, proteostasis, and mitochondrial dynamics. We translated the workflow to human studies, creating a reference dataset of 496 plasma protein turnover rates from 4 healthy adults. The approach is applicable to short, minimal label enrichment and can be performed on as little as a single biopsy, thereby overcoming critical obstacles to clinical investigations. The protein turnover quantitation experiments and computational workflow described here should be widely applicable to large-scale biomolecular investigations of human disease mechanisms with a temporal perspective.

Indexed as

Adrenergic beta-AgonistsAdultAnimalsCalcium SignalingDeuterium OxideHeartHeart FailureHumansIsoproterenolKineticsMaleMass SpectrometryMiceMice, Inbred ICRMitochondria, HeartMuscle ProteinsAdrenergic beta-AgonistsDeuterium OxideIsoproterenolMuscle ProteinsProteins

Identifiers

PMID24614109
PMCPMC3973111
OpenAlexW2167799942

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.