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Systemic Proteomic Alterations and Predictive Biomarkers of Paroxetine Response in Refractory Rosacea : A Secondary Analysis of a Randomized Clinical Trial
Systemic Proteomic Alterations and Predictive Biomarkers of Paroxetine Response in Refractory Rosacea: A Secondary Analysis of a Randomized Clinical Trial Key Points Question What are the systemic molecular mechanisms underlying the therapeutic efficacy of paroxetine in patients with refractory erythematous rosacea, and can protein biomarkers be identified to predict clinical response?
Metabolite-gated vascular contractility switch: OXGR1 activation mechanism enables agonist therapy for rosacea erythema
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Keywords rosacea oxoglutaric acid OXGR1 cryo-EM vasodilation Get full text access Log in, subscribe or purchase for full access. References 1. Gether, L. ∙ Overgaard, L.K. ∙ Egeberg, A. ... Incidence and prevalence of rosacea: a systematic review and meta-analysis Br. J. Dermatol. 2018; 179:282-289 2. Aksoy, B. ∙ Altaykan-Hapa, A. ∙ Egemen, D. ... The impact of rosacea on quality of life: effects of demographic and clinical characteristics and various treatment modalities Br. J. Dermatol. 2010; 163:719-725 3.
By Wenqin Xiao, Yan Zhu, Xinjie Jonathan Tang, Kongkai Zhu, Weifeng Zhang, Mengting Chen, Kui Cai, Zheng Wu, Mei Wang, JIAYI LIU, Zixin Tan, Zhixiang Zhao, Yan Tang, Yingxue Huang, Ben Wang, Fangfen Liu, Qian Wang, Fan Yang, Dan Jian, Wei Shi, Hongfu Xie, Xiang Chen, Lulu guo, Zhili Deng, Jinpeng Sun, Ji Li, San Xu, Linglong Long, Aike Wu, Songqi Zhou
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Cell Press
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Frontiers | The impact of Jinlida on blood glucose control and insulin resistance in patients with prediabetes and type 2 diabetes: a systematic review and meta-analysis of randomized controlled trials
SYSTEMATIC REVIEW article Volume 16 - 2025 | https://doi.org/10.3389/fendo.2025.1689640 This article is part of the Research TopicReviews in Clinical Diabetes and HealthcareView all 14 articles 1 Introduction Type 2 diabetes mellitus (T2DM) is a chronic and progressive metabolic disorder characterized by sustained hyperglycemia that disrupts the normal metabolism of glucose, lipids, and proteins.
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