ArticleCell death & disease2016
Nogo-C regulates cardiomyocyte apoptosis during mouse myocardial infarction.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Transcriptomic profiles of susceptibility and resilience to stress in the amygdala and hippocampus of male rats.Neurobiology of stress · 2025Article
- MicroRNA delivery based on nanoparticles of cardiovascular diseases.Molecular and cellular biochemistry · 2024Review
- Article
- Nogo-A Mediated Endoplasmic Reticulum Stress During Myocardial Ischemic-Reperfusion Injury in Diabetic Rats.Cardiovascular toxicology · 2023Article
- Nogo-A and LINGO-1: Two Important Targets for Remyelination and Regeneration.International journal of molecular sciences · 2023Review
- Role of miR-182 in cardiovascular and cerebrovascular diseases.Frontiers in cell and developmental biology · 2023Review
- miR-182-5p Regulates Nogo-A Expression and Promotes Neurite Outgrowth of Hippocampal Neurons In Vitro.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Nogo-B promotes angiogenesis and improves cardiac repair after myocardial infarction via activating Notch1 signaling.Cell death & disease · 2022Article
- Article
- Nogo-A regulates myogenesis via interacting with Filamin-C.Cell death discovery · 2021Article
- Myocardial Infarction: The Protective Role of MiRNAs in Myocardium Pathology.Frontiers in cardiovascular medicine · 2021Review
- Endophilin A2-mediated alleviation of endoplasmic reticulum stress-induced cardiac injury involves the suppression of ERO1α/IPInternational journal of biological sciences · 2021Article
- miRNA-182/Deptor/mTOR axis regulates autophagy to reduce intestinal ischaemia/reperfusion injury.Journal of cellular and molecular medicine · 2020Article
- Nogo-C Inhibits Peripheral Nerve Regeneration by Regulating Schwann Cell Apoptosis and Dedifferentiation.Frontiers in neuroscience · 2020Article
- Translationally controlled tumor protein (TCTP) plays a pivotal role in cardiomyocyte survival through a Bnip3-dependent mechanism.Cell death & disease · 2019Article
- Nogo-B promotes tumor angiogenesis and provides a potential therapeutic target in hepatocellular carcinoma.Molecular oncology · 2018Article
- Histamine deficiency aggravates cardiac injury through miR-206/216b-Atg13 axis-mediated autophagic-dependant apoptosis.Cell death & disease · 2018Article
- Nogo-C regulates post myocardial infarction fibrosis through the interaction with ER CaCell death & disease · 2018Article
- Stress Coping Strategies in the Heart: An Integrated View.Frontiers in cardiovascular medicine · 2018Review
- Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial infarction is caused by insufficient coronary blood supply, which leads to myocardial damage and eventually the heart failure. Molecular mechanisms associated with the loss of cardiomyocytes during myocardial infarction (MI) and ischemia-related cardiac diseases are not yet fully understood. Nogo-C is an endoplasmic reticulum protein ubiquitously expressed in tissues including in the heart, however, the cardiac function of Nogo-C is still unknown. In the present study, we found that Nogo-C was upregulated in mouse hearts after MI, and hypoxic treatments also increased Nogo-C protein level in cardiomyocytes. Adenovirus mediated overexpression of Nogo-C led to cardiomyocyte apoptosis, whereas knockdown of Nogo-c by shRNA protected cardiomyocytes from hypoxia-induced cell apoptosis. Importantly, Nogo-C knockout mice displayed improved cardiac function, smaller infarct area, and less apoptotic cells after MI. Moreover, we found that miR-182 negatively regulated Nogo-C expression and was downregulated during MI, expressing miR-182 in cardiomyocytes protected hypoxia- and Nogo-C-mediated cell apoptosis. Our results indicate that increased cardiac Nogo-C expression is both sufficient and necessary for ischemia-induced cardiomyocyte apoptosis and cardiac dysfunction, suggesting that deregulation of Nogo-C by miRNA may be a potential therapeutic target for ischemia-related heart diseases.
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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.