ArticleCell stress & chaperones2009
NGFI-B targets mitochondria and induces cardiomyocyte apoptosis in restraint-stressed rats by mediating energy metabolism disorder.
Article in Cell stress & chaperones, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 13 citations in OpenAlex.
- Decline of cardiomyocyte contractile performance and bioenergetic function in socially stressed male rats.Heliyon · 2022Article
- Advances in understanding mechanisms and therapeutic targets to treat comorbid depression and cardiovascular disease.Neuroscience and biobehavioral reviews · 2020Review
- Effect of sepsis on the action potential and cardiac serotonin response in rats.Experimental and therapeutic medicine · 2019Article
- HSP70 inhibits stress-induced cardiomyocyte apoptosis by competitively binding to FAF1.Cell stress & chaperones · 2015Article
- Article
- A neuroendocrine mechanism of co-morbidity of depression-like behavior and myocardial injury in rats.PloS one · 2014Article
- Mitochondrial translocation of Nur77 mediates cardiomyocyte apoptosis.European heart journal · 2011Article
- Expression of uncoupling protein 3 in mitochondria protects against stress-induced myocardial injury: a proteomic study.Cell stress & chaperones · 2010Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NGFI-B/Nur77/TR3, originally identified as an immediate-early gene rapidly induced by serum and growth factors, is a member of the steroid hormone nuclear receptor superfamily with no identified endogenous ligand. NGFI-B induces apoptosis in a number of cell lineages exposed to proapoptotic stimuli by directly targeting the mitochondria, inducing cytochrome c release. The present study was designed to determine the role of NGFI-B in cardiomyocytes of restraint-stressed rats. The NGFI-B content was increased in mitochondria and reduced in plasma as apoptosis increased. Analysis showed that NGFI-B induces cardiomyocyte apoptosis in restraint-stressed rats by mediating mitochondrial energy metabolism disorder. Several novel mitochondrial proteins, which correlate with NGFI-B, were reported in cardiomyocyte apoptosis of restraint-stressed rats. Five proteins associated with NGFI-B participate directly in mitochondrial energy metabolism. Studies of mitochondrial respiratory efficiency and ATP synthase activity strongly support the findings. These results provide significant information for comprehensively understanding the cellular mechanism of cardiovascular diseases.
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Registered trials
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