ArticleProceedings of the National Academy of Sciences of the United States of America2000
Conditional expression of a Gi-coupled receptor causes ventricular conduction delay and a lethal cardiomyopathy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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Who cites it
47 citing papers in PubMed, 169 citations in OpenAlex.
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- Matricellular proteins in cutaneous wound healing.Frontiers in cell and developmental biology · 2022Review
- Reverse Remodeling With Left Ventricular Assist Devices.Circulation research · 2021Review
- The GPR17 Receptor-A Promising Goal for Therapy and a Potential Marker of the Neurodegenerative Process in Multiple Sclerosis.International journal of molecular sciences · 2020Review
- Association of Autoantibodies against M2-Muscarinic Acetylcholine Receptor with Atrial Fibrosis in Atrial Fibrillation Patients.Cardiology research and practice · 2019Article
- Resolving Behavioral Output via Chemogenetic Designer Receptors Exclusively Activated by Designer Drugs.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Review
- DREADDs for Neuroscientists.Neuron · 2016Review
- A selective review of robust variable selection with applications in bioinformatics.Briefings in bioinformatics · 2015Review
- Gαi/o-coupled receptor signaling restricts pancreatic β-cell expansion.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- DREADDs: novel tools for drug discovery and development.Drug discovery today · 2014Review
- Abnormal muscle mechanosignaling triggers cardiomyopathy in mice with Marfan syndrome.The Journal of clinical investigation · 2014Article
- Proteomic analysis of human placental syncytiotrophoblast microvesicles in preeclampsia.Clinical proteomics · 2014Article
- Disrupted bone remodeling leads to cochlear overgrowth and hearing loss in a mouse model of fibrous dysplasia.PloS one · 2014Article
- Rodent models of heart failure: an updated review.Heart failure reviews · 2013Review
- Plasma concentrations of extracellular matrix protein fibulin-1 are related to cardiovascular risk markers in chronic kidney disease and diabetes.Cardiovascular diabetology · 2013Article
- Plasma fibulin-1 is linked to restrictive filling of the left ventricle and to mortality in patients with aortic valve stenosis.Journal of the American Heart Association · 2012Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
Cardiomyopathy is a major cause of morbidity and mortality. Ventricular conduction delay, as shown by prolonged deflections in the electrocardiogram caused by delayed ventricular contraction (wide QRS complex), is a common feature of cardiomyopathy and is associated with a poor prognosis. Although the G(i)-signaling pathway is up-regulated in certain cardiomyopathies, previous studies suggested this up-regulation was compensatory rather than a potential cause of the disease. Using the tetracycline transactivator system and a modified G(i)-coupled receptor (Ro1), we provide evidence that increased G(i) signaling in mice can result in a lethal cardiomyopathy associated with a wide QRS complex arrhythmia. Induced expression of Ro1 in adult mice resulted in a >90% mortality rate at 16 wk, whereas suppression of Ro1 expression after 8 wk protected mice from further mortality and allowed partial improvement in systolic function. Results of DNA-array analysis of over 6,000 genes from hearts expressing Ro1 are consistent with hyperactive G(i) signaling. DNA-array analysis also identified known markers of cardiomyopathy and hundreds of previously unknown potential diagnostic markers and therapeutic targets for this syndrome. Our system allows cardiomyopathy to be induced and reversed in adult mice, providing an unprecedented opportunity to dissect the role of G(i) signaling in causing cardiac pathology.
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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.