ArticleProteomics2009
Proteomic profiling of KATP channel-deficient hypertensive heart maps risk for maladaptive cardiomyopathic outcome.
Article in Proteomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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.
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.
Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Proteomics of the heart.Physiological reviews · 2024Review
- KScientific reports · 2022Article
- Ischemic Heart Disease and Heart Failure: Role of Coronary Ion Channels.International journal of molecular sciences · 2020Review
- Cardiopoietic stem cell therapy restores infarction-altered cardiac proteome.NPJ Regenerative medicine · 2020Article
- Mitochondrial proteome remodeling in ischemic heart failure.Life sciences · 2014Article
- Effects of hypertension and exercise on cardiac proteome remodelling.BioMed research international · 2014Review
- Systems proteomics for translational network medicine.Circulation. Cardiovascular genetics · 2012Article
- Measuring and evaluating the role of ATP-sensitive K+ channels in cardiac muscle.Journal of molecular and cellular cardiology · 2012Review
- Investigating the secretome: lessons about the cells that comprise the heart.Circulation. Cardiovascular genetics · 2012Article
- Advances in cardiac ATP-sensitive K+ channelopathies from molecules to populations.Circulation. Arrhythmia and electrophysiology · 2011Article
- K(ATP) channel-dependent metaboproteome decoded: systems approaches to heart failure prediction, diagnosis, and therapy.Cardiovascular research · 2011Review
- ATP-sensitive K(+) channel-deficient dilated cardiomyopathy proteome remodeled by embryonic stem cell therapy.Stem cells (Dayton, Ohio) · 2010Article
- Human K(ATP) channelopathies: diseases of metabolic homeostasis.Pflugers Archiv : European journal of physiology · 2010Review
- Muscle KATP channels: recent insights to energy sensing and myoprotection.Physiological reviews · 2010Review
- Sub-proteomic fractionation, iTRAQ, and OFFGEL-LC-MS/MS approaches to cardiac proteomics.Journal of proteomics · 2010Article
- Proteomics and mass spectrometry: what have we learned about the heart?Current cardiology reviews · 2010Article
- Glycolytic network restructuring integral to the energetics of embryonic stem cell cardiac differentiation.Journal of molecular and cellular cardiology · 2010Article
- Cardiogenic induction of pluripotent stem cells streamlined through a conserved SDF-1/VEGF/BMP2 integrated network.PloS one · 2010Article
- Quaternary structure of KATP channel SUR2A nucleotide binding domains resolved by synchrotron radiation X-ray scattering.Journal of structural biology · 2010Article
- KATP channel Kir6.2 E23K variant overrepresented in human heart failure is associated with impaired exercise stress response.Human genetics · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
KCNJ11 null mutants, lacking Kir6.2 ATP-sensitive K(+) (K(ATP)) channels, exhibit a marked susceptibility towards hypertension (HTN)-induced heart failure. To gain insight into the molecular alterations induced by knockout of this metabolic sensor under hemodynamic stress, wild-type (WT) and Kir6.2 knockout (Kir6.2-KO) cardiac proteomes were profiled by comparative 2-DE and Orbitrap MS. Despite equivalent systemic HTN produced by chronic hyperaldosteronism, 114 unique proteins were altered in Kir6.2-KO compared to WT hearts. Bioinformatic analysis linked the primary biological function of the K(ATP) channel-dependent protein cohort to energetic metabolism (64% of proteins), followed by signaling infrastructure (36%) including oxidoreductases, stress-related chaperones, processes supporting protein degradation, transcription and translation, and cytostructure. Mapped protein-protein relationships authenticated the primary impact on metabolic pathways, delineating the K(ATP) channel-dependent subproteome within a nonstochastic network. Iterative systems interrogation of the proteomic web prioritized heart-specific adverse effects, i.e., "Cardiac Damage", "Cardiac Enlargement", and "Cardiac Fibrosis", exposing a predisposition for the development of cardiomyopathic traits in the hypertensive Kir6.2-KO. Validating this maladaptive forecast, phenotyping documented an aggravated myocardial contractile performance, a massive interstitial fibrosis and an exaggerated left ventricular size, all prognostic indices of poor outcome. Thus, Kir6.2 ablation engenders unfavorable proteomic remodeling in hypertensive hearts, providing a composite molecular substrate for pathologic stress-associated cardiovascular disease.
Indexed as
Identifiers
What OpenQuestion holds
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.