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Retinal cell survival pathways" is not a specific molecule or receptor but rather refers to a collection of intracellular signaling cascades and molecular mechanisms that regulate the survival and death of retinal cells, particularly retinal ganglion cells. These pathways include the phosphoinositide 3‑kinase (PI3K)/AKT pathway, mitogen‑activated protein kinase (MAPK) pathway—including ERK, p38 MAPK, and JNK/c-Jun branches—and the Bcl‑2 family–mediated mitochondrial apoptosis pathway. Dysregulation of these pathways contributes to retinal diseases such as glaucoma by promoting programmed cell death (apoptosis) in response to stressors like increased intraocular pressure or ischemia. Therapeutic strategies often aim to modulate these signaling networks—such as enhancing CREB/BCL2 activity or inhibiting pro-apoptotic signals—to protect against vision loss by preserving retinal neuron viability[1][2][3]. The entry "Retinal cell survival pathways" does not refer to a single canonical target molecule or receptor but instead encompasses multiple molecular processes and proteins involved in maintaining the viability of various retinal neurons. Therefore, it is not considered a therapeutic target in the conventional sense; rather, individual components within these pathways may serve as drug targets[1][2][3].
Activation of neuroprotective signaling pathways such as PI3K/AKT, MAPK, and CREB/BCL2 to prevent apoptosis in retinal ganglion cells
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