ArticleScientific reports2024
rESWT promoted angiogenesis via Bach1/Wnt/β-catenin signaling pathway.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- More than a ring: the emerging role of heme in angiogenesis.Cell communication and signaling : CCS · 2026Review
- Toward function-oriented, neuroscience-based spine care in older adults: a structured narrative review and translational synthesis.Frontiers in pain research (Lausanne, Switzerland) · 2026Review
- Extracorporeal shock wave therapy alleviates glucocorticoid-induced injury and dysfunction of bone microvascular endothelial cells via the PI3K/AKT/FOXO1 pathway.Annals of joint · 2026Article
- MiR-503-5p as a potential biomarker for deep venous thrombosis (DVT) in multiple myeloma (MM) and its role in disease development.Annals of hematology · 2025Article
- Identification of angiogenesis-related hub genes in proliferative diabetic retinopathy via integrated transcriptomics and machine learning.Diabetology & metabolic syndrome · 2025Article
- The Multifaceted Roles of BACH1 in Disease: Implications for Biological Functions and Therapeutic Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
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Authors and funding
5 authors.
Funding
Abstract
Previous reports have established that rESWT fosters angiogenesis, yet the mechanism by which rESWT promotes cerebral angiogenesis remains elusive. rESWT stimulated HUVECs proliferation as evidenced by the CCK-8 test, with an optimal dosage of 2.0 Bar, 200 impulses, and 2 Hz. The tube formation assay of HUVECs revealed that tube formation peaked at 36 h post-rESWT treatment, concurrent with the lowest expression level of Bach1, as detected by both Western blot and immunofluorescence. The expression level of Wnt3a, β-catenin, and VEGF also peaked at 36 h. A Bach1 overexpression plasmid was transfected into HUVECs, resulting in a decreased expression level of Wnt3a, β-catenin, and VEGF. Upon treatment with rESWT, the down-regulation of Wnt3a, β-catenin, and VEGF expression in the transfected cells was reversed. The Wnt/β-catenin inhibitor DKK-1 was utilized to suppress Wnt3a and β-catenin expression, which led to a concurrent decrease in VEGF expression. However, rESWT treatment could restore the expression of these three proteins, even in the presence of DKK-1. Moreover, in the established OGD model, it was observed that rESWT could inhibit the overexpression of Bach1 and enhance VEGF and VEGFR-2 expression under the OGD environment.
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Registered trials
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