ArticleAmerican journal of physiology. Renal physiology2014
Semaphorin 3A inactivation suppresses ischemia-reperfusion-induced inflammation and acute kidney injury.
Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 52 citations in OpenAlex.
- Cidea Targeting Protects Cochlear Hair Cells and Hearing Function From Drug- and Noise-Induced Damage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Acute Kidney Injury Biomarkers in Perioperative Care: A Scoping Review of Clinical Implementation.Diagnostics (Basel, Switzerland) · 2025Review
- Evaluation of a Novel Biomarker Panel for Acute Kidney Injury Following Endovascular Aortic Repair.International journal of molecular sciences · 2025Article
- The Role of Immune Semaphorins in Sepsis-A Prospective Cohort Study.Microorganisms · 2024Article
- Adhesion G Protein-Coupled ReceptorCells · 2024Article
- Soluble Neuropilin-1 Is Elevated in Sepsis and Correlates with Organ Dysfunction and Long-Term Mortality in Critical Illness.International journal of molecular sciences · 2024Article
- Adriamycin-induced podocyte injury via the Sema3A/TRPC5/Rac1 pathway.Frontiers in medicine · 2024Article
- Role of Semaphorin 3A in Kidney Development and Diseases.Diagnostics (Basel, Switzerland) · 2023Review
- Sema3A Drives Alternative Macrophage Activation in the Resolution of Periodontitis via PI3K/AKT/mTOR Signaling.Inflammation · 2023Article
- Delayed Contralateral Nephrectomy Halted Post-Ischemic Renal Fibrosis Progression and Inhibited the Ischemia-Induced Fibromir Upregulation in Mice.Biomedicines · 2021Article
- The Role of Semaphorins and Their Receptors in Innate Immune Responses and Clinical Diseases of Acute Inflammation.Frontiers in immunology · 2021Review
- Semaphorin3A-Inhibitor Ameliorates Doxorubicin-Induced Podocyte Injury.International journal of molecular sciences · 2020Article
- Semaphorin 3F Promotes Transendothelial Migration of Leukocytes in the Inflammatory Response After Survived Cardiac Arrest.Inflammation · 2019Article
- Rapamycin induces autophagy to alleviate acute kidney injury following cerebral ischemia and reperfusion via the mTORC1/ATG13/ULK1 signaling pathway.Molecular medicine reports · 2018Article
- Inhibition of semaphorin-3a suppresses lipopolysaccharide-induced acute kidney injury.Journal of molecular medicine (Berlin, Germany) · 2018Article
- Gpr97 Exacerbates AKI by Mediating Sema3A Signaling.Journal of the American Society of Nephrology : JASN · 2018Article
- Urinary semaphorin 3A as an early biomarker to predict contrast-induced acute kidney injury in patients undergoing percutaneous coronary intervention.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018Article
- Netrins & Semaphorins: Novel regulators of the immune response.Biochimica et biophysica acta. Molecular basis of disease · 2017Review
- Epoxide metabolites of arachidonate and docosahexaenoate function conversely in acute kidney injury involved in GSK3β signaling.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Cardiac surgery-associated acute kidney injury: risk factors, pathophysiology and treatment.Nature reviews. Nephrology · 2017Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Recent studies show that guidance molecules that are known to regulate cell migration during development may also play an important role in adult pathophysiologic states. One such molecule, semaphorin3A (sema3A), is highly expressed after acute kidney injury (AKI) in mice and humans, but its pathophysiological role is unknown. Genetic inactivation of sema3A protected mice from ischemia-reperfusion-induced AKI, improved tissue histology, reduced neutrophil infiltration, prevented epithelial cell apoptosis, and increased cytokine and chemokine excretion in urine. Pharmacological-based inhibition of sema3A receptor binding likewise protected against ischemia-reperfusion-induced AKI. In vitro, sema3A enhanced toll-like receptor 4-mediated inflammation in epithelial cells, macrophages, and dendritic cells. Moreover, administration of sema3A-treated, bone marrow-derived dendritic cells exacerbated kidney injury. Finally, sema3A augmented cisplatin-induced apoptosis in kidney epithelial cells in vitro via expression of DFFA-like effector a (cidea). Our data suggest that the guidance molecule sema3A exacerbates AKI via promoting inflammation and epithelial cell apoptosis.
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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.