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"Reduce tissue cell death" refers to the therapeutic aim of limiting pathological cell loss in tissues, often by modulating molecular pathways of programmed cell death such as apoptosis, necroptosis, ferroptosis, and autophagy. Excessive cell death underlies many diseases (cancer, ischemia, neurodegeneration, inflammation), and multiple drug classes have been developed to target the molecules that regulate these processes. However, as this is a process or effect, not a specific molecular target, its application as a therapeutic target requires identification of specific receptors, enzymes, or proteins involved in the cell death pathways most relevant to the disease context[1][3][5][7]. This entry should not be used as a structured molecular target but as a starting point for identifying specific pathways or molecules involved in tissue cell death. Direct mapping to current databases or drug development pipelines requires specification of molecular entities (e.g., "BCL2", "Caspase 3", "Tumor necrosis factor receptor 1", etc.), not broad biological effects.
Inhibition of apoptotic pathways (e.g., blocking caspase activity, BCL2 interactions); Inhibition of necroptosis or ferroptosis (e.g., iron chelation, lipid peroxidation blockers); Modulation of autophagy (activation or inhibition); Targeting death receptors or downstream signaling (e.g., DR5, Fas)
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