AbstractObjective. Anabolic androgenic steroids (AAS) may exert effects through the insulin-like growth factor (IGF) system. We compared the IGF system in

Recent research highlights how Stanniocalcin-1 could be crucial in treating idiopathic pulmonary arterial hypertension by inhibiting vascular remodeling.

特発性肺動脈性肺高血圧症に関する東京医科大学と岡山大学の研究で、Stanniocalcin-1が治療に役立つ可能性が示されました。

特発性肺動脈性肺高血圧症の新たな研究成果が示す可能性。血管保護因子Stanniocalcin-1の役割と今後の治療に期待。

2026.09.11 東京医科大学,岡山大学 プレスリリース 【概要】東京医科大学(学長:宮澤啓介/東京都新宿区)細胞生理学分野 横山詩子主任教授、呼吸器内科学分野 ...

Calreticulin-mediated activation of immunogenic cell death (ICD) is hindered by stanniocalcin-1 (STC1), which blocks its surface translocation. Here, the authors report the antitumor immune benefits of STC1 silencing and present a nanoplatform co-delivering siSTC1 and the ICD inducer paclitaxel in Lewis lung carcinoma models.

A novel mechanism of colonic epithelial damage and parthanatos in patients with Crohn's disease (CD) is proposed. STC1 mediates oxidative stress-associated parthanatos and aggravates inflammation via the STC1-PARP1-JNK interactions and subsequent JNK pathway activation in CD pathogenesis. The study provides a potential therapy for the alleviation of colitis. Abstract Stanniocalcin-1 (STC1) is upregulated by inflammation and modulates oxidative stress-induced cell death. Herein, the function of STC1 in colitis and stress-induced parthanatos, a newly identified type of programmed necrotic cell death dependent on the activation of poly-ADP ribose polymerase-1 (PARP1) is investigated. Results show that STC1 expression is markedly increased in the inflamed colonic mucosa of Crohn's disease (CD) patients and chemically-induced mice colitis models. Evaluation of parthanatos severity and pro-inflammatory cytokine expression shows that intestinal-specific Stc1 knockout ( Stc1 INT-KO ) mice are resistant to dextran sulfate sodium (DSS)-induced colitis and exhibit lower disease severity. STC1-overexpressing cells show an increased degree of parthanatos and proinflammatory cytokine expression, whereas STC1-knockout cells show a decreased degree of parthanatos. Co-immunoprecipitation, mass spectrometry, and proteomic analyses indicate that STC1 interacts with PARP1, which activates the JNK pathway via PARP1–JNK interactions. Moreover, inhibition of PARP1 and JNK alleviates parthanatos and inflammatory injuries triggered by STC1 overexpression. Finally, following restoration of Stc1 and Parp1 expression by adeno-associated viruses, and overexpression of Stc1 and Parp1 aggravated DSS-induced colitis in Stc1 INT-KO mice. In conclusion, STC1 mediates oxidative stress-associated parthanatos and aggravates inflammation via the STC1–PARP1–JNK interactions and subsequent JNK pathway activation in CD pathogenesis.