ArticleBMC cardiovascular disorders2022
SERPINB1 overexpression protects myocardial damage induced by acute myocardial infarction through AMPK/mTOR pathway.
Article in BMC cardiovascular disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
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- SerpinB1a induces hepatopulmonary syndrome by promoting CTSG/AMPK/mTOR pathway-mediated mitophagy.Cell biology and toxicology · 2025Article
- Changes in the Dentate Gyrus Gene Expression Profile Induced by Levetiracetam Treatment in Rats with Mesial Temporal Lobe Epilepsy.International journal of molecular sciences · 2024Article
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSERPINB1 is involved in the development of a variety of diseases. The purpose of this study was to explore the effect of SERPINB1 on acute myocardial infarction (AMI).
methodsSerum SERPINB1 level of AMI patients was measured for receiver operating characteristic curve analysis. The AMI rat model was constructed to observe myocardial damage, and the H9C2 cell oxygen glucose deprivation (OGD) model was constructed to detect cell viability. Transthoracic echocardiography was used to assess the cardiac function. TTC staining and HE staining were used to detect pathologic changes of myocardial tissues. The apoptosis of myocardial tissues and cells were measured by TUNLE staining and flow cytometry assay. CCK-8 assay to measure cell viability. SERPINB1 expression was measured by qRT-PCR. Protein expression was measured by western blot.
resultsThe serum SERPINB1 level was down-regulated in AMI patients. AMI modeling reduced the SERPINB1 expression level, induced inflammatory cells infiltrated, and myocardial apoptosis. OGD treatment inhibited cell viability and promoted apoptosis. The AMPK/mTOR pathway was inhibited in AMI rats and OGD-treated H9C2 cells. Overexpression of SERPINB1 reduced infarct size and myocardial apoptosis of AMI rats, inhibited apoptosis of H9C2 cells, and activated AMPK/mTOR pathway. However, AMPK inhibitor Dorsomorphin reversed the protective effect of SERPINB1 on myocardial cells.
conclusionSERPINB1 overexpression relieved myocardial damage induced by AMI via AMPK/mTOR pathway.
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