ArticleScientific reports2017
Loss of MD1 exacerbates pressure overload-induced left ventricular structural and electrical remodelling.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 40 citations in OpenAlex.
- Targeting the Ubiquitin-Proteasome System in Atrial Fibrillation: Mechanistic Insights and Translational Perspectives.Current issues in molecular biology · 2025Review
- USP38 exacerbates pressure overload-induced left ventricular electrical remodeling.Molecular medicine (Cambridge, Mass.) · 2024Article
- LY86 facilitates ox-LDL-induced lipid accumulation in macrophages by upregulating SREBP2/HMGCR expression.BMC cardiovascular disorders · 2024Article
- Ubiquitin specific protease 38 aggravates pathological cardiac remodeling by stabilizing phospho-TBK1.International journal of biological sciences · 2024Article
- Effects of Phenylacetylglutamine on the Susceptibility of Atrial Fibrillation in Overpressure-Induced HF Mice.Molecular and cellular biology · 2024Article
- Ubiquitin-specific protease 38 promotes inflammatory atrial fibrillation induced by pressure overload.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2023Article
- Deficiency of inhibitory TLR4 homolog RP105 exacerbates fibrosis.JCI insight · 2022Article
- Identification of key differential genes in intimal hyperplasia induced by left carotid artery ligation.PeerJ · 2022Article
- The Intriguing Role of TLR Accessory Molecules in Cardiovascular Health and Disease.Frontiers in cardiovascular medicine · 2022Review
- The Akt pathway mediates the protective effects of myeloid differentiation protein 1 in pathological cardiac remodelling.ESC heart failure · 2021Article
- The Potential Role of RP105 in Regulation of Inflammation and Osteoclastogenesis During Inflammatory Diseases.Frontiers in cell and developmental biology · 2021Review
- Article
- MD1 deletion exaggerates cardiomyocyte autophagy induced by heart failure with preserved ejection fraction through ROS/MAPK signalling pathway.Journal of cellular and molecular medicine · 2020Article
- Article
- Loss of myeloid differentiation protein 1 promotes atrial fibrillation in heart failure with preserved ejection fraction.ESC heart failure · 2020Article
- Key Player in Cardiac Hypertrophy, Emphasizing the Role of Toll-Like Receptor 4.Frontiers in cardiovascular medicine · 2020Review
- The effect of MD1 on potassium and L-type calcium current of cardiomyocytes from high-fat diet mice.Channels (Austin, Tex.) · 2020Article
- MD-1 Deficiency Accelerates Myocardial Inflammation and Apoptosis in Doxorubicin-Induced Cardiotoxicity by Activating the TLR4/MAPKs/Nuclear Factor kappa B (NF-κB) Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Myeloid differentiation protein 1 protected myocardial function against high-fat stimulation induced pathological remodelling.Journal of cellular and molecular medicine · 2019Article
- MicroRNA-145 Protects against Myocardial Ischemia Reperfusion Injury via CaMKII-Mediated Antiapoptotic and Anti-Inflammatory Pathways.Oxidative medicine and cellular longevity · 2019Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myeloid differentiation protein 1 (MD1) has been implicated in numerous pathophysiological processes, including immune regulation, obesity, insulin resistance, and inflammation. However, the role of MD1 in cardiac remodelling remains incompletely understood. We used MD1-knockout (KO) mice and their wild-type littermates to determine the functional significance of MD1 in the regulation of aortic banding (AB)-induced left ventricular (LV) structural and electrical remodelling and its underlying mechanisms. After 4 weeks of AB, MD1-KO hearts showed substantial aggravation of LV hypertrophy, fibrosis, LV dilation and dysfunction, and electrical remodelling, which resulted in overt heart failure and increased electrophysiological instability. Moreover, MD1-KO-AB cardiomyocytes showed increased diastolic sarcoplasmic reticulum (SR) Ca
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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.