ArticleCell death & disease2021
Cardiac-specific CGI-58 deficiency activates the ER stress pathway to promote heart failure in mice.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
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- Identification of transcription factor-lipid droplet-related gene biomarkers for the prognosis of post-acute myocardial infarction-induced heart failure.Frontiers in cardiovascular medicine · 2024Article
- Article
- The multifaceted roles of ER and Golgi in metabolic cardiomyopathy.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Excess myocardial triacylglycerol accumulation (i.e., cardiac steatosis) impairs heart function, suggesting that enzymes promoting triacylglycerol metabolism exert essential regulatory effects on heart function. Comparative gene identification 58 (CGI-58) is a key enzyme that promotes the hydrolysis of triglycerides by activating adipose triglyceride lipase and plays a protective role in maintaining heart function. In this study, the effects of CGI-58 on heart function and the underlying mechanism were investigated using cardiac-specific CGI58-knockout mice (CGI-58
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Registered trials
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