ArticleOxidative medicine and cellular longevity2016
CD38 Deficiency Protects the Heart from Ischemia/Reperfusion Injury through Activating SIRT1/FOXOs-Mediated Antioxidative Stress Pathway.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 2 of them syntheses that pooled it.
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Who cites it
56 citing papers in PubMed, 2 syntheses or guidelines pooled it, 84 citations in OpenAlex.
- Unveiling the role of NAD glycohydrolase CD38 in aging and age-related diseases: insights from bibliometric analysis and comprehensive review.Frontiers in immunology · 2025Pooled it
- Risk of thromboembolism in patients with multiple myeloma treated with daratumumab: a systemic review and meta-analysis.International journal of hematology · 2020Pooled it
- Chasing the FoxO in Metabolic Disorders: Novel Considerations for Oxidative Stress, Programmed Cell Death, Wnt, and the Gut Microbiome.Antioxidants (Basel, Switzerland) · 2026Review
- Circulating CD38 shows stronger association with incident heart failure in women despite lower levels: sex differences and kidney-function context.Biology of sex differences · 2026Article
- Perioperative immune dynamics during cardiopulmonary bypass and association with major adverse postoperative events.Frontiers in cardiovascular medicine · 2026Article
- CD38-NAD(+) Axis: New Insights into Glaucoma Therapy.Molecular neurobiology · 2025Review
- Phospholipase C epsilon 1 as a therapeutic target in cardiovascular diseases.Journal of advanced research · 2025Review
- CD38 connects the heart and brain.Translational psychiatry · 2025Review
- The role of sirtuins in the regulation of reactive oxygen species in myocardial ischemia/reperfusion injury.Molecular and cellular biochemistry · 2025Review
- Cardiomyocyte specific CD38 deletion protects heart from acute myocardial infarction by activating Sirt3 signaling pathway.Scientific reports · 2025Article
- Myeloid but not hepatocytic CD38 is a key driver for hepatic ischemia/reperfusion injury.Signal transduction and targeted therapy · 2025Article
- The Role of NADAmerican journal of cardiovascular drugs : drugs, devices, and other interventions · 2025Review
- Emerging interactions between mitochondria and NADTrends in endocrinology and metabolism: TEM · 2025Review
- Sodium butyrate protect bone mass in lipopolysaccharide-treated rats by reducing oxidative stress and inflammatory.Redox report : communications in free radical research · 2024Article
- NADCell communication and signaling : CCS · 2024Review
- NAD metabolism and heart failure: Mechanisms and therapeutic potentials.Journal of molecular and cellular cardiology · 2024Review
- Smooth-Muscle-Cell-Specific Deletion of CD38 Protects Mice from AngII-Induced Abdominal Aortic Aneurysm through Inhibiting Vascular Remodeling.International journal of molecular sciences · 2024Article
- O-GlcNAcylation mediates HActa pharmacologica Sinica · 2024Article
- NAD in pathological cardiac remodeling: Metabolic regulation and beyond.Biochimica et biophysica acta. Molecular basis of disease · 2024Review
- SIRT1 safeguards adipogenic differentiation by orchestrating anti-oxidative responses and suppressing cellular senescence.GeroScience · 2024Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Ischemia/reperfusion (I/R) injury induces irreversible oxidative stress damage to the cardiac muscle. We previously observed that CD38 deficiency remarkably protects mouse embryonic fibroblasts (MEFs) from oxidative stress-induced injury. However, whether CD38 deficiency protects from I/R injury in the heart is not explored. Here, we showed that the hearts of CD38 deficient mice or wild type mice supplied with exogenous NAD were significantly protected from ischemia/reperfusion injury, seen as reduction of the myocardial infarct sizes when the mice were subjected to 30 min ischemia followed by 24 hours of reperfusion. Consistently, the protection of CD38 deficiency on hypoxia/reoxygenation (H/R) injury was confirmed with a CD38 knockdown H9c2 stable cell line. Furthermore, we observed that knockdown of CD38 remarkably inhibited ROS generation and intracellular Ca(2+) overloading induced by H/R in H9c2 cells. The FOXO1 and FOXO3 expressions were significantly elevated by H/R injury in CD38 knockdown cells compared with normal H9c2 cells. The cell immunofluorescence assay showed that FOXO1 nuclear translocation was significantly increased in CD38 knockdown H9c2 cells. In addition, we demonstrated that the increase of FOXO1 nuclear translocation was associated with the increased expressions of antioxidant catalase and SOD2 and the attenuated expression of the ROS generation enzyme NOX4. In conclusion, our results provide new evidence that CD38 deficiency protects the heart from I/R injury through activating SIRT1/FOXOs-mediated antioxidative stress pathway.
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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.