ArticlePloS one2019
Protective role of the deSUMOylating enzyme SENP3 in myocardial ischemia-reperfusion injury.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- New Insights into TFEB SUMOylation and Its Role in Lipid Metabolism and Cardiovascular Disease.International journal of molecular sciences · 2025Review
- Effects of Cytokines (or Activating Factors) on Arterial Endothelial Cells.International journal of molecular sciences · 2025Review
- SENP3 alleviates osteoporosis via promoting SIRT3 transcription through the increase of DLX2 stability via SUMO2/3.Cell biology and toxicology · 2025Article
- Mendelian randomization provides a multi-omics perspective on the regulation of genes involved in ribosome biogenesis in relation to cardiac structure and function.Clinical epigenetics · 2025Article
- SENP3-FIS1 axis promotes mitophagy and cell survival under hypoxia.Cell death & disease · 2024Article
- Exploring the Role of Unconventional Post-Translational Modifications in Cancer Diagnostics and Therapy.Current protein & peptide science · 2024Review
- SENP3-mediated deSUMOylation of c-Jun facilitates microglia-induced neuroinflammation after cerebral ischemia and reperfusion injury.iScience · 2023Article
- The role of SUMOylation in the neurovascular dysfunction after acquired brain injury.Frontiers in pharmacology · 2023Review
- SENP3 Aggravates Renal Tubular Epithelial Cell Apoptosis in Lipopolysaccharide-Induced Acute Kidney Injury via deSUMOylation of Drp1.Kidney diseases (Basel, Switzerland) · 2022Article
- ATF3 in atherosclerosis: a controversial transcription factor.Journal of molecular medicine (Berlin, Germany) · 2022Review
- SUMOylation targeting mitophagy in cardiovascular diseases.Journal of molecular medicine (Berlin, Germany) · 2022Review
- SUMOylation does not affect cardiac troponin I stability but alters indirectly the development of force in response to CaThe FEBS journal · 2022Article
- Effects of amyloid-β on protein SUMOylation and levels of mitochondrial proteins in primary cortical neurons.IBRO neuroscience reports · 2022Article
- The Function of SUMOylation and Its Critical Roles in Cardiovascular Diseases and Potential Clinical Implications.International journal of molecular sciences · 2021Review
- SUMO-specific Isopeptidases Tuning Cardiac SUMOylation in Health and Disease.Frontiers in molecular biosciences · 2021Review
- Profiling the Murine SUMO Proteome in Response to Cardiac Ischemia and Reperfusion Injury.Molecules (Basel, Switzerland) · 2020Article
- Review
- Ginkgetin Alleviates Inflammation, Oxidative Stress, and Apoptosis Induced by Hypoxia/Reoxygenation in H9C2 Cells via Caspase-3 Dependent Pathway.BioMed research international · 2020Article
- The Critical Roles of the SUMO-Specific Protease SENP3 in Human Diseases and Clinical Implications.Frontiers in physiology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Interruption of blood supply to the heart is a leading cause of death and disability. However, the molecular events that occur during heart ischemia, and how these changes prime consequent cell death upon reperfusion, are poorly understood. Protein SUMOylation is a post-translational modification that has been strongly implicated in the protection of cells against a variety of stressors, including ischemia-reperfusion. In particular, the SUMO2/3-specific protease SENP3 has emerged as an important determinant of cell survival after ischemic infarct. Here, we used the Langendorff perfusion model to examine changes in the levels and localisation of SUMOylated target proteins and SENP3 in whole heart. We observed a 50% loss of SENP3 from the cytosolic fraction of hearts after preconditioning, a 90% loss after ischemia and an 80% loss after ischemia-reperfusion. To examine these effects further, we performed ischemia and ischemia-reperfusion experiments in the cardiomyocyte H9C2 cell line. Similar to whole hearts, ischemia induced a decrease in cytosolic SENP3. Furthermore, shRNA-mediated knockdown of SENP3 led to an increase in the rate of cell death upon reperfusion. Together, our results indicate that cardiac ischemia dramatically alter levels of SENP3 and suggest that this may a mechanism to promote cell survival after ischemia-reperfusion in heart.
Indexed as
Identifiers
What OpenQuestion holds
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.