Corrigendum to “Echistatin/BYL-719 impedes epithelial-mesenchymal transition in pulmonary fibrosis induced by silica through modulation of the Integrin β1/ILK/PI3K signaling pathway” [Int. Immunopharmacol. 136 (2024) 112368]

Author: Feng, Kaihao ; Zhou, Qiang ; Chang, Meiyu ; Xu, Shushuo ; Li, Haibin ; Wang, Penghao ; Yao, Sanqiao ; Li, Xinxiao ; Hu, Meng ; Xu, Deliang

01 Jul 2024·International Immunopharmacology

Echistatin/BYL-719 impedes epithelial-mesenchymal transition in pulmonary fibrosis induced by silica through modulation of the Integrin β1/ILK/PI3K signaling pathway

Article

Author: Feng, Kaihao ; Zhou, Qiang ; Xu, Shushuo ; Chang, Meiyu ; Li, Haibin ; Wang, Penghao ; Yao, Sanqiao ; Li, Xinxiao ; Hu, Meng ; Xu, Deliang

Silicosis is a chronic fibroproliferative lung disease caused by long-term inhalation of crystalline silica dust, characterized by the proliferation of fibroblasts and pulmonary interstitial fibrosis. Currently, there are no effective treatments available. Recent research suggests that the Integrin β1/ILK/PI3K signaling pathway may be associated with the pathogenesis of silicosis fibrosis. In this study, we investigated the effects of Echistatin (Integrin β1 inhibitor) and BYL-719 (PI3K inhibitor) on silicosis rats at 28 and 56 days after silica exposure. Histopathological analysis of rat lung tissue was performed using H&E staining and Masson staining. Immunohistochemistry, Western blotting, and qRT-PCR were employed to assess the expression of markers associated with epithelial-mesenchymal transition (EMT), fibrosis, and the Integrin β1/ILK/PI3K pathway in lung tissue. The results showed that Echistatin, BYL 719 or their combination up-regulated the expression of E-cadherin and down-regulated the expression of Vimentin and extracellular matrix (ECM) components, including type I and type III collagen. The increase of Snail, AKT and β-catenin in the downstream Integrin β1/ILK/PI3K pathway was inhibited. These results indicate that Echistatin and BYL 719 can inhibit EMT and pulmonary fibrosis by blocking different stages of Integrinβ1 /ILK/PI3K signaling pathway. This indicates that the Integrin β1/ILK/PI3K signaling pathway is associated with silica-induced EMT and may serve as a potential therapeutic target for silicosis.

01 Jan 2024·Odontology

Effect of ELVAX polymer subgingival implants with echistatin on extracted and reimplanted rats’ teeth

Article

Author: Garcia, Roberto Brandao ; Leite, Milena Gomes Melo ; Pinheiro, Tiago Novaes ; Faria, Flavio Duarte ; Bramante, Clovis Monteiro ; Pinheiro, Bethania Camargo ; Cintra, Luciano Tavares Angelo ; Bernardineli, Norberti

To investigate the effect of ELVAX polymer subgingival implants incorporated with echistatin peptide on incisor reimplanted tooth in rats. Forty-two male Wistars rats were divided into two groups: echistatin-treated rats (E) and control rats (C). The animals had their right maxillary incisors extracted and treated according to the International Association of Dental Traumatology replantation protocol. The extra-alveolar dry period was 30 and 60 min, and the post-surgical experimental periods were 15, 60, and 90 days. The samples were stained with H&E and analyzed for the presence of an inflammatory response, incidence of resorptions, and dental ankylosis. Results were statistically analyzed (p < 0.05). The presence of inflammatory resorption was significantly higher in group C at 30 and 60 min extra-alveolar time, in the 15-day postoperative period as compared with the E group (p < 0.05). Dental ankylosis was significantly more prevalent in group E in 30 min extra-alveolar time and 15 days postoperative period (p < 0.05). However, in 60 min extra-alveolar time and 60 days postoperative period, dental ankylosis was more prevalent in C group (p < 0.05). The use of ELVAX subgingival implants with echistatin demonstrated therapeutic potential in preventing the experimental resorption process after replantation of maxillary incisors in rats.

100 Deals associated with Echistatin

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Indication	Highest Phase	Country/Location	Organization	Date
Myocardial Ischemia	Phase 2	-	Merck Sharp & Dohme Corp.	-
Myocardial Ischemia	Phase 2	US	Merck GmbH	-
Myocardial Ischemia	Phase 2	-	Merck Sharp & Dohme Corp.	-
Myocardial Ischemia	Phase 2	US	Merck GmbH	-
Thrombosis	Phase 2	US	Merck GmbH	-
Thrombosis	Phase 2	US	Merck GmbH	-
Thrombosis	Phase 2	-	Merck Sharp & Dohme Corp.	-
Thrombosis	Phase 2	-	Merck Sharp & Dohme Corp.	-
Osteosarcoma	Preclinical	US	AntiCancer, Inc.	15 Apr 2012

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