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| 1 | Waixenicin A,a marine-derived TRPM7 inhibitor:a promising CNS drug lead显示文摘Ion channels are the third largest class of targets for therapeutic drugs.The pharmacology of ion channels is an important research area for identifying new treatment options for human diseases.The past decade or so has seen increasing interest in an ion channel protein belonging to the transient receptor potential(TRP)family,namely the melastatin subfamily member 7(TRPM7),as an emerging drug target.TRPM7 is a bifunctional protein with a magnesium and calcium-conducting divalent ion channel fused with an active kinase domain.TRPM7 is ubiquitously expressed in human tissues,including the brain,and regulates various cell biology processes such as magnesium and calcium homeostasis,cell growth and proliferation,and embryonic development.TRPM7 provides a link between cellular metabolic status and intracellular calcium homeostasis in neurons due to TRPM7’s unique sensitivity to fluctuating intracellular Mg·ATP levels.Thus,the protein plays a key role in ischemic and hypoxic neuronal cell death and brain injury,and is one of the key nonglutamate mechanisms in cerebral ischemia and stroke.Currently,the most potent and specific TRPM7 inhibitor is waixenicin A,a xenicane diterpenoid from the Hawaiian soft coral Sarcothelia edmondsoni.Using waixenicin A as a pharmacological tool,we demonstrated that TRPM7 is involved in promoting neurite outgrowth in vitro.Most recently,we found that waixenicin A reduced hypoxic-ischemic brain injury and preserved long-term behavioral outcomes in mouse neonates.We here suggest that TRPM7 is an emerging drug target for CNS diseases and disorders,and waixenicin A is a viable drug lead for these disorders. | Hong-Shuo Sun F.David Horgen Daniel Romo Kenneth G.Hull Sigrid A.Kiledal Andrea Fleig Zhong-Ping Feng | 2020 | Acta Pharmacologica Sinica2020，41，12： | 2 |
| 2 | 氯离子通道与缺血性卒中显示文摘缺血性卒中是发病率和致残率最高的疾病之一。高血压是公认的缺血性卒中最重要的独立危险因素,在高血压发展过程中出现的血管重构是引发缺血性卒中的病理学基础。研究表明,血管平滑肌细胞异常增殖和凋亡都将导致血管重构。此外,脑缺血再灌注可导致神经元损伤和凋亡。近来的研究表明,血管重构和神经元凋亡都与氯离子通道有关。至少3种氯离子通道参与这些过程:容积调控的氯离子通道、钙激活的氯离子通道以及囊性纤维跨膜电导调节体。文章就这3种氯离子通道在血管重构、神经元凋亡以及缺血性卒中中的作用进行了综述。 | 曹翔 徐运 | 2017 | 国际脑血管病杂志2017，25，3： | 2 |
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