ArticleThe Journal of clinical investigation2008
Parasympathetic response in chick myocytes and mouse heart is controlled by SREBP.
Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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Who cites it
22 citing papers in PubMed, 168 citations in OpenAlex.
- SREBP1 Transactivation of NHE3 Impairs Cardiac Contraction and Aggravates Heart Failure.Circulation · 2026Article
- Bioengineered peptibodies as blockers of ion channels.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Article
- Novel cholesterol-dependent regulation of cardiac KPhysiological reports · 2021Article
- SREBP1 regulates mitochondrial metabolism in oncogenic KRAS expressing NSCLC.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Article
- Developmental and extrahepatic physiological functions of SREBP pathway genes in mice.Seminars in cell & developmental biology · 2018Review
- Article
- Histone deacetylase inhibitors modulate KATP subunit transcription in HL-1 cardiomyocytes through effects on cholesterol homeostasis.Frontiers in pharmacology · 2015Article
- Glycogen synthase kinase-3β inhibition ameliorates cardiac parasympathetic dysfunction in type 1 diabetic Akita mice.Diabetes · 2014Article
- Acetylcholinesterase (AChE) inhibition aggravates fasting-induced triglyceride accumulation in the mouse liver.FEBS open bio · 2014Article
- Increased inducibility of ventricular tachycardia and decreased heart rate variability in a mouse model for type 1 diabetes: effect of pravastatin.American journal of physiology. Heart and circulatory physiology · 2013Article
- Gene expression profiles in engineered cardiac tissues respond to mechanical loading and inhibition of tyrosine kinases.Physiological reports · 2013Article
- MuMoD: a Bayesian approach to detect multiple modes of protein-DNA binding from genome-wide ChIP data.Nucleic acids research · 2013Article
- Expanding roles for SREBP in metabolism.Cell metabolism · 2012Review
- The relationship among brain natriuretic peptide (BNP), cholesterol and lipoprotein.Heart Asia · 2012Article
- Fatty acid synthase modulates homeostatic responses to myocardial stress.The Journal of biological chemistry · 2011Article
- Role of NMDA receptor-dependent activation of SREBP1 in excitotoxic and ischemic neuronal injuries.Nature medicine · 2009Article
- Genome-wide analysis of SREBP-1 binding in mouse liver chromatin reveals a preference for promoter proximal binding to a new motif.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Role of SREBP-1 in the development of parasympathetic dysfunction in the hearts of type 1 diabetic Akita mice.Circulation research · 2009Article
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 3 countries.
Funding
Abstract
Parasympathetic stimulation of the heart, which provides protection from arrhythmias and sudden death, involves activation of the G protein-coupled inward rectifying K+ channel GIRK1/4 and results in an acetylcholine-sensitive K+ current, I KACh. We describe a unique relationship between lipid homeostasis, the lipid-sensitive transcription factor SREBP-1, regulation of the cardiac parasympathetic response, and the development of ventricular arrhythmia. In embryonic chick atrial myocytes, lipid lowering by culture in lipoprotein-depleted serum increased SREBP-1 levels, GIRK1 expression, and I KACh activation. Regulation of the GIRK1 promoter by SREBP-1 and lipid lowering was dependent on interaction with 2 tandem sterol response elements and an upstream E-box motif. Expression of dominant negative SREBP-1 (DN-SREBP-1) reversed the effect of lipid lowering on I KACh and GIRK1. In SREBP-1 knockout mice, both the response of the heart to parasympathetic stimulation and the expression of GIRK1 were reduced compared with WT. I KACh, attenuated in atrial myocytes from SREBP-1 knockout mice, was stimulated by SREBP-1 expression. Following myocardial infarction, SREBP-1 knockout mice were twice as likely as WT mice to develop ventricular tachycardia in response to programmed ventricular stimulation. These results demonstrate a relationship between lipid metabolism and parasympathetic response that may play a role in arrhythmogenesis.
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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.