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| 1 | Pharmacological insights into autophagy modulation in autoimmune diseases显示文摘As a cellular bulk degradation and survival mechanism,autophagy is implicated in diverse biological processes.Genome-wide association studies have revealed the link between autophagy gene polymorphisms and susceptibility of autoimmune diseases including systemic lupus erythematosus(SLE)and inflammatory bowel disease(IBD),indicating that autophagy dysregulation may be involved in the development of autoimmune diseases.A series of autophagy modulators have displayed protective effects on autoimmune disease models,highlighting the emerging role of autophagy modulators in treating autoimmune diseases.This review explores the roles of autophagy in the autoimmune diseases,with emphasis on four major autoimmune diseases[SLE,rheumatoid arthritis(RA),IBD,and experimental autoimmune encephalomyelitis(EAE)].More importantly,the therapeutic potentials of small molecular autophagy modulators(including autophagy inducers and inhibitors)on autoimmune diseases are comprehensively analyzed. | Ming-Yue Wu Er-Jin Wang Du Feng Min Li Richard D.Ye Jia-Hong Lu | 2021 | Acta Pharmaceutica Sinica B2021，11，11： | 7 |
| 2 | Corynoxine B targets at HMGB1/2 to enhance autophagy forα-synuclein clearance in fly and rodent models of Parkinson's disease显示文摘Parkinson's disease(PD)is the most common neurodegenerative movement disease.It is featured by abnormal alphα-synuclein(α-syn)aggregation in dopaminergic neurons in the substantia nigra.Macroautophagy(autophagy)is an evolutionarily conserved cellular process for degradation of cellular contents,including protein aggregates,to maintain cellular homeostasis.Corynoxine B(Cory B),a natural alkaloid isolated from Uncaria rhynchophylla(Miq.)Jacks.,has been reported to promote the clearance ofα-syn in cell models by inducing autophagy.However,the molecular mechanism by which Cory B induces autophagy is not known,and theα-syn-lowering activity of Cory B has not been verified in animal models.Here,we report that Cory B enhanced the activity of Beclin 1/VPS34 complex and increased autophagy by promoting the interaction between Beclin 1 and HMGB1/2.Depletion of HMGB1/2 impaired Cory B-induced autophagy.We showed for the first time that,similar to HMGB1,HMGB2 is also required for autophagy and depletion of HMGB2 decreased autophagy levels and phosphatidylinositol 3-kinaseⅢactivity both under basal and stimulated conditions.By applying cellular thermal shift assay,surface plasmon resonance,and molecular docking,we confirmed that Cory B directly binds to HMGB1/2 near the C106 site.Furthermore,in vivo studies with a wild-typeα-syn transgenic drosophila model of PD and an A53Tα-syn transgenic mouse model of PD,Cory B enhanced autophagy,promotedα-syn clearance and improved behavioral abnormalities.Taken together,the results of this study reveal that Cory B enhances phosphatidylinositol 3-kinaseⅢactivity/autophagy by binding to HMGB1/2 and that this enhancement is neuroprotective against PD. | Qi Zhu Juxian Song Jia-Yue Chen Zhenwei Yuan Liangfeng Liu Li-Ming Xie Qiwen Liao Richard D.Ye Xiu Chen Yepiao Yan Jieqiong Tan Chris Soon Heng Tan Min Li Jia-Hong Lu | 2023 | Acta Pharmaceutica Sinica B2023，13，6： | 2 |
| 3 | A TELEMONITORING NETWORK:DESIGN AND CLINICAL TEST显示文摘 | J.Bai Y.Zhang B.Dai J.Lin Z.Zhu Z.Cui J.Zhang P.Zhang D.Shen S.Yao S.Cd D.Ye | 1995 | Chinese Journal of Biomedical Engineering(English Edition)1995，4，2： | 0 |
| 4 | Anti-inflammatory signaling through G protein-coupled receptors显示文摘G protein-coupled receptors(GPCRs)play important roles in human physiology.GPCRs are involved in immunoregulation including regulation of the inflammatory response.Chemotaxis of phagocytes and lymphocytes is mediated to a great extent by the GPCRs for chemoattractants including myriads of chemokines.Accumulation and activation of phagocytes at the site of inflammation contribute to local inflammatory response.A handful of GPCRs have been found to transduce anti-inflammatory signals that promote resolution of inflammation.These GPCRs interact with selected metabolites of arachdonic acid,such as lipoxins,and of omega-3 essential fatty acids,such as resolvins and protectins.Despite mounting evidence for the in vivo functions of these anti-inflammatory and pro-resolving ligands paired with their respective GPCRs,the underlying signaling mechanisms have not been fully delineated.The present review summarizes what we have learned about these GPCRs,their structures and signaling pathways and the prospect of targeting these receptors for novel anti-inflammatory therapies. | Yun-jun Ge Qi-wen Liao Ye-chun Xu Qiang Zhao Bei-li Wu Richard D.Ye | 2020 | Acta Pharmacologica Sinica2020，41，12： | 0 |
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