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Literature summary for 1.6.3.1 extracted from
- Cardiac oxidative stress and remodeling following infarction: role of NADPH oxidase (2008), Cardiovasc. Pathol., 18, 156-166.
Application
| Application | Comment | Organism |
|---|---|---|
| medicine | wild-type mice with myocardial infarction display significantly increased gp91phox and 3-nitrotyrosine in the infarcted myocardium, accumulated macrophages and myofibroblasts at the infarct site, abundant apoptotic myocytes primarily at border zones on day 3, and numerous apoptotic inflammatory/myofibroblasts in the later stages. Transforming growth factor 1, tissue inhibitor of metalloprotease 2, and type 1 collagen gene expression is increased, collagen volume in the infarcted myocardium continuously increases, and noninfarcted myocardium displays hypertrophy. Compared to wild-type mice with myocardial infarction, subunit gp91phox knockout mice do not display significant difference in infarct size/thickness, cardiac hypertrophy, myocyte apoptosis, inflammatory/fibrogenic responses, as well as cardiac oxidative stress | Mus musculus |
Protein Variants
| Protein Variants | Comment | Organism |
|---|---|---|
| additional information | compared to wild-type mice with myocardial infarction, subunit gp91phox knockout mice do not display significant difference in infarct size/thickness, cardiac hypertrophy, myocyte apoptosis, inflammatory/fibrogenic responses, as well as cardiac oxidative stress | Mus musculus |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Mus musculus | - |
- |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| heart | - |
Mus musculus | - |
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Release 2023.1 (January 2023)
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