ArticleCardiovascular research2016
Acute heart failure with cardiomyocyte atrophy induced in adult mice by ablation of cardiac myosin light chain kinase.
Article in Cardiovascular research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
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- Novel cardiac myosin inhibitor for hypertrophic cardiomyopathy.The Journal of general physiology · 2024Article
- Loss of cardiac myosin light chain kinase contributes to contractile dysfunction in right ventricular pressure overload.Physiological reports · 2022Article
- Myosin Light Chain Kinase Modulates to Improve Myocardial Hypoxia/Reoxygenation Injury.Journal of healthcare engineering · 2022Article
- Proteomics study on the effect of silybin on cardiomyopathy in obese mice.Scientific reports · 2021Article
- Aging Attenuates Cardiac Contractility and Affects Therapeutic Consequences for Myocardial Infarction.Aging and disease · 2020Review
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- Novel Invasive and Noninvasive Cardiac-Specific Biomarkers in Obesity and Cardiovascular Diseases.Metabolic syndrome and related disorders · 2020Review
- Cardiac MLC2 kinase is localized to the Z-disc and interacts with α-actinin2.Scientific reports · 2019Article
- Impact of cardiac myosin light chain kinase gene mutation on development of dilated cardiomyopathy.ESC heart failure · 2019Article
- Down-regulation of miR-200c attenuates AngII-induced cardiac hypertrophy via targeting the MLCK-mediated pathway.Journal of cellular and molecular medicine · 2019Article
- HeterozygousFrontiers in physiology · 2019Article
- Lycium barbarum polysaccharides restore adverse structural remodelling and cardiac contractile dysfunction induced by overexpression of microRNA-1.Journal of cellular and molecular medicine · 2018Article
- Pressure Overload-induced Cardiac Hypertrophy Varies According to Different Ligation Needle Sizes and Body Weights in Mice.Arquivos brasileiros de cardiologia · 2018Article
- miR-133: A Suppressor of Cardiac Remodeling?Frontiers in pharmacology · 2018Review
- Natural genetic variation of the cardiac transcriptome in non-diseased donors and patients with dilated cardiomyopathy.Genome biology · 2017Article
- Pseudophosphorylation of cardiac myosin regulatory light chain: a promising new tool for treatment of cardiomyopathy.Biophysical reviews · 2017Review
- Role of myosin light chain phosphatase in cardiac physiology and pathophysiology.Journal of molecular and cellular cardiology · 2016Review
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
aimsUnder pressure overload, initial adaptive hypertrophy of the heart is followed by cardiomyocyte elongation, reduced contractile force, and failure. The mechanisms governing the transition to failure are not fully understood. Pressure overload reduced cardiac myosin light chain kinase (cMLCK) by ∼80% within 1 week and persists. Knockdown of cMLCK in cardiomyocytes resulted in reduced cardiac contractility and sarcomere disorganization. Thus, we hypothesized that acute reduction of cMLCK may be causative for reduced contractility and cardiomyocyte remodelling during the transition from compensated to decompensated cardiac hypertrophy. METHODS AND
resultsTo mimic acute cMLCK reduction in adult hearts, the floxed-Mylk3 gene that encodes cMLCK was inducibly ablated in Mylk3(flox/flox)/merCremer mice (Mylk3-KO), and compared with two control mice (Mylk3(flox/flox) and Mylk3(+/+)/merCremer) following tamoxifen injection (50 mg/kg/day, 2 consecutive days). In Mylk3-KO mice, reduction of cMLCK protein was evident by 4 days, with a decline to below the level of detection by 6 days. By 7 days, these mice exhibited heart failure, with reduction of fractional shortening compared with those in two control groups (19.8 vs. 28.0% and 27.7%). Severely convoluted cardiomyocytes with sarcomeric disorganization, wavy fibres, and cell death were demonstrated in Mylk3-KO mice. The cardiomyocytes were also unable to thicken adaptively to pressure overload.
conclusionOur results, using a new mouse model mimicking an acute reduction of cMLCK, suggest that cMLCK plays a pivotal role in the transition from compensated to decompensated hypertrophy via sarcomeric disorganization.
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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.