ArticleInternational journal of molecular sciences2020
Semaphorin3A-Inhibitor Ameliorates Doxorubicin-Induced Podocyte Injury.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Elucidation of puberulic acid-induced nephrotoxicity using stem cell-based kidney organoids.Scientific reports · 2025Article
- Semaphorin3A Rewires CD4International journal of molecular sciences · 2025Article
- Naringin mitigated doxorubicin-induced kidney injury by the reduction of oxidative stress and inflammation with a synergistic anticancer effect.BMC pharmacology & toxicology · 2025Article
- Article
- The Abl1 tyrosine kinase is a key player in doxorubicin-induced cardiomyopathy and its p53/p73 cell death mediated signaling differs in atrial and ventricular cardiomyocytes.Journal of translational medicine · 2024Article
- Biological role of Semaphorin 6D in the proliferation, migration and invasion of gastric cancer.African health sciences · 2024Article
- Role of biophysics and mechanobiology in podocyte physiology.Nature reviews. Nephrology · 2024Review
- 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
- Pancreatic cancer cell-derived semaphorin 3A promotes neuron recruitment to accelerate tumor growth and dissemination.American journal of cancer research · 2023Article
- KCNQ1OT1 inhibition alleviates high glucose-induced podocyte injury by adsorbing miR-23b-3p and regulating Sema3A.Clinical and experimental nephrology · 2022Article
- Diabetes and Its Cardiovascular Complications: Comprehensive Network and Systematic Analyses.Frontiers in cardiovascular medicine · 2022Review
- Doxorubicin-Induced Fetal Mesangial Cell Death Occurs Independently of TRPC6 Channel Upregulation but Involves Mitochondrial Generation of Reactive Oxygen Species.International journal of molecular sciences · 2021Article
- MicroRNAs as Biomarkers for Nephrotic Syndrome.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Podocyte injury is an independent risk factor for the progression of renal diseases. Semaphorin3A (SEMA3A), expressed in podocytes and tubular cells in the mammalian adult kidneys, has been reported to regulate diverse biological functions and be associated with renal diseases. Here, we investigated pathological roles of SEMA3A signaling on podocyte injury using a doxorubicin (Dox)-induced mouse model and examined the therapeutic effect of SEMA3A-inhibitor (SEMA3A-I). We demonstrated that Dox caused massive albuminuria and podocyte apoptosis as well as an increase of SEMA3A expression in podocytes, all of which were ameliorated with SEMA3A-I treatment. In addition, c-Jun N-terminal kinase (JNK), known as a downstream of SEMA3A signaling, was activated in Dox-injected mouse podocytes while SEMA3A-I treatment partially blocked the activation. In vitro, SEMA3A-I protected against Dox-induced podocyte apoptosis and recombinant SEMA3A caused podocyte apoptosis with activation of JNK signaling. JNK inhibitor, SP600125, attenuated SEMA3A-induced podocyte apoptosis, indicating that the JNK pathway would be involved in SEMA3A-induced podocyte apoptosis. Furthermore, the analysis of human data revealed a positive correlation between levels of urinary SEMA3A and protein, suggesting that SEMA3A is associated with podocyte injury. In conclusion, SEMA3A has essential roles in podocyte injury and it would be the therapeutic target for protecting from podocyte injury.
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