期刊
APOPTOSIS
卷 14, 期 4, 页码 469-477出版社
SPRINGER
DOI: 10.1007/s10495-008-0304-8
关键词
Apoptosis; Necroptosis; Necrosis; Stroke; Neurodegeneration
资金
- NIH [DP1OD000580]
- National Institute of Neurological Disorders and Stroke [UO1 NS050560]
- National Institute on Aging [R37-AG012859, PO1 AG027916]
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [U01NS050560] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P01AG027916, R37AG012859] Funding Source: NIH RePORTER
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [DP1OD000580] Funding Source: NIH RePORTER
It has been a major challenge to develop effective therapeutics for stroke, a leading cause of death and serious debilitation. Intensive research in the past 15 years have implicated many regulators and the related mechanisms by which neuronal cell death is regulated. It is now clear that even a brief ischemic stroke may trigger complex cellular events that lead to both apoptotic and necrotic neuronal cell death in a progressive manner. Although efforts at developing specific chemical inhibitors for validated targets have been successful for in vitro enzymatic assays, the development of some of such inhibitors into human therapy has been often hindered by their in vivo bioavailability profile. Considerations for the ability to chemically target a cellular mechanism in manner compatible with disease targets in vivo might be emphasized early in the development process by putting a priority on identifying key targets that can be effectively targeted chemically. Thorough interrogation of cellular pathways by saturation chemical genetics may provide a novel strategy to identify multiple key molecular entities that can be targeted chemically in order to select a target suitable for the treatment of intended human diseases such as stroke.
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