ArticleExperimental and therapeutic medicine2016
LSKL peptide alleviates subarachnoid fibrosis and hydrocephalus by inhibiting TSP1-mediated TGF-β1 signaling activity following subarachnoid hemorrhage in rats.
Article in Experimental and therapeutic medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Systematic Review of the Differential Effects of TGF-β1 in Ischemic and Hemorrhagic Preclinical Stroke Models.Journal of the American Heart Association · 2025Pooled it
- Proteomics and human microchips identify Thrombospondin-1 as a potential biomarker for calciphylaxis stem cell therapy.iScience · 2026Article
- Serum Biomarkers in Paediatric Neurosurgery: Traumatic Brain Injury and Beyond.Advances and technical standards in neurosurgery · 2026Article
- Blocking TSP1 Ameliorates Diabetes Mellitus-Induced Erectile Dysfunction by Inhibiting the TGF-β/SMAD Pathway.The world journal of men's health · 2025Article
- Hydrocephalus: Molecular and Neuroimaging Biomarkers in Diagnosis and Management.Biomedicines · 2025Review
- Meningeal lymphatic drainage: novel insights into central nervous system disease.Signal transduction and targeted therapy · 2025Review
- Interplay Between TGFβ1 Signaling and Cancer-Testis Antigen MAGEB2: A New Thorn in Cancer's Side?International journal of molecular sciences · 2025Article
- The transcription factor TCF4 regulates the miR-494-3p/THBS1 axis in the fibrosis of pathologic scars.Archives of dermatological research · 2025Article
- Advancing Hydrocephalus Management: Pathogenesis Insights, Therapeutic Innovations, and Emerging Challenges.Aging and disease · 2024Review
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- Increased thrombospondin-1 levels contribute to epileptic susceptibility in neonatal hyperthermia without seizures via altered synaptogenesis.Cell death discovery · 2024Article
- Review
- Genetic and molecular mechanisms of hydrocephalus.Frontiers in molecular neuroscience · 2024Review
- Animal Welfare Aspects in Planning and Conducting Experiments on Rodent Models of Subarachnoid Hemorrhage.Cellular and molecular neurobiology · 2023Review
- Inflammatory Markers as Predictors of Shunt Dependency and Functional Outcome in Patients with Aneurysmal Subarachnoid Hemorrhage.Biomedicines · 2023Article
- Irradiation induces DJ-1 secretion from esophageal squamous cell carcinoma cells to accelerate metastasis of bystander cells via a TGF-β1 positive feedback loop.Journal of experimental & clinical cancer research : CR · 2022Article
- Runt related transcription factor-1 plays a central role in vessel co-option of colorectal cancer liver metastases.Communications biology · 2021Article
- The Pathogenesis of Hydrocephalus Following Aneurysmal Subarachnoid Hemorrhage.International journal of molecular sciences · 2021Review
- Article
- Efficacy of antibiotic-impregnated shunt versus conventional shunts to reduce cerebrospinal fluid infections in children: A systematic review and meta-analysis.Experimental and therapeutic medicine · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hydrocephalus has been demonstrated to be an independent risk factor for poor outcomes in patients with subarachnoid hemorrhage (SAH). Blockage of cerebrospinal fluid (CSF) flow and drainage is widely considered to play a vital role in communicating hydrocephalus, possibly due to subarachnoid fibrosis. A previous study indicated that transforming growth factor-β1 (TGF-β1), a key fibrogenic factor, is significantly increased in the CSF following SAH, implying a pivotal role in the development of chronic hydrocephalus. To investigate whether LSKL peptide, a small molecular peptide and competitive antagonist for TGF-β1, protects against subarachnoid fibrosis and hydrocephalus after SAH, a two-hemorrhage injection model of SAH was created in Sprague-Dawley rats. LSKL (1 mg/kg) was administered intraperitoneally immediately following the first intravenous injection of blood in the SAH model, with repeated injections of LSKL every 12 h until sacrifice. Thrombospondin-1 (TSP1), TGF-β1, p-Smad2/3, collagen I and pro-collagen I c-terminal propeptide levels were assessed via western blotting and ELISA. Lateral ventricular index, Masson staining and Morris water maze tests were employed to evaluate subarachnoid fibrosis, hydrocephalus and long-term neurological function following SAH. It was found that the LKSL peptide readily crossed the blood brain barrier, was protective against subarachnoid fibrosis, attenuated ventriculomegaly and effectively suppressed hydrocephalus. In addition, the results indicated that the protective effects of the LSKL peptide were achieved via the inhibition of TGF-β1 activity and subsequent Smad2/3 signaling. Importantly, the LSKL peptide may improve long-term neurocognitive deficits after SAH. In conclusion, the LSKL peptide suppresses subarachnoid fibrosis via inhibition of TSP1-mediated TGF-β1 activity, prevents the development of chronic hydrocephalus and improves long-term neurocognitive defects following SAH.
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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.