ArticleThe EMBO journal2003
Cellular remodeling in heart failure disrupts K(ATP) channel-dependent stress tolerance.
Article in The EMBO journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 89 citations in OpenAlex.
- Immune dysregulation as a key driver of peripartum cardiomyopathy - an exploratory advanced imaging and biomarker study.European journal of heart failure · 2025Article
- Heart failure, inflammation and exercise.International journal of biological sciences · 2025Review
- KScientific reports · 2022Article
- The role of extracellular vesicles in regulating local and systemic inflammation in cardiovascular disease.Pharmacological research · 2021Review
- Reappraising the role of inflammation in heart failure.Nature reviews. Cardiology · 2020Review
- Ectopic overexpression of Kir6.1 in the mouse heart impacts on the life expectancy.Scientific reports · 2018Article
- ATP sensitive potassium channel openers: A new class of ocular hypotensive agents.Experimental eye research · 2017Review
- Article
- Disruption of ATP-sensitive potassium channel function in skeletal muscles promotes production and secretion of musclin.Biochemical and biophysical research communications · 2016Article
- Article
- Isosteviol Sensitizes sarcKATP Channels towards Pinacidil and Potentiates Mitochondrial Uncoupling of Diazoxide in Guinea Pig Ventricular Myocytes.Oxidative medicine and cellular longevity · 2016Article
- Disruption of KATP channel expression in skeletal muscle by targeted oligonucleotide delivery promotes activity-linked thermogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2015Article
- LKB1 knockout mouse develops spontaneous atrial fibrillation and provides mechanistic insights into human disease process.Journal of the American Heart Association · 2015Article
- Sarcolemmal ATP-sensitive potassium channels modulate skeletal muscle function under low-intensity workloads.The Journal of general physiology · 2014Article
- Disrupting KATP channels diminishes the estrogen-mediated protection in female mutant mice during ischemia-reperfusion.Clinical proteomics · 2014Article
- Mechanical dyssynchrony precedes QRS widening in ATP-sensitive K⁺ channel-deficient dilated cardiomyopathy.Journal of the American Heart Association · 2013Article
- Kir6.2 limits Ca(2+) overload and mitochondrial oscillations of ventricular myocytes in response to metabolic stress.American journal of physiology. Heart and circulatory physiology · 2013Article
- Tumor necrosis factor receptor-associated factor 2 signaling provokes adverse cardiac remodeling in the adult mammalian heart.Circulation. Heart failure · 2013Article
- Regulation of cardiac ATP-sensitive potassium channel surface expression by calcium/calmodulin-dependent protein kinase II.The Journal of biological chemistry · 2013Article
- Heterogeneous upregulation of apamin-sensitive potassium currents in failing human ventricles.Journal of the American Heart Association · 2013Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
ATP-sensitive potassium (K(ATP)) channels are required for maintenance of homeostasis during the metabolically demanding adaptive response to stress. However, in disease, the effect of cellular remodeling on K(ATP) channel behavior and associated tolerance to metabolic insult is unknown. Here, transgenic expression of tumor necrosis factor alpha induced heart failure with typical cardiac structural and energetic alterations. In this paradigm of disease remodeling, K(ATP) channels responded aberrantly to metabolic signals despite intact intrinsic channel properties, implicating defects proximal to the channel. Indeed, cardiomyocytes from failing hearts exhibited mitochondrial and creatine kinase deficits, and thus a reduced potential for metabolic signal generation and transmission. Consequently, K(ATP) channels failed to properly translate cellular distress under metabolic challenge into a protective membrane response. Failing hearts were excessively vulnerable to metabolic insult, demonstrating cardiomyocyte calcium loading and myofibrillar contraction banding, with tolerance improved by K(ATP) channel openers. Thus, disease-induced K(ATP) channel metabolic dysregulation is a contributor to the pathobiology of heart failure, illustrating a mechanism for acquired channelopathy.
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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.