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Neuroprotective therapies for glaucoma.

Song W, Huang P, Zhang C - Drug Des Devel Ther (2015)

Bottom Line: However, it has been found that progressive GON is still present in some patients with effective IOP decrease.Therefore, risk factors other than IOP elevation, like neurotrophin deprivation and excitotoxicity, contribute to progressive GON.Novel approaches of neuroprotection may be more effective for preserving the function of the optic nerve.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Peking University Third Hospital, Beijing, People's Republic of China.

ABSTRACT
Glaucoma is the second leading cause for blindness worldwide. It is mainly caused by glaucomatous optic neuropathy (GON) characterized by retinal ganglion cell loss, which leads to visual field defect and blindness. Up to now, the main purpose of antiglaucomatous therapies has been to lower intraocular pressure (IOP) through surgeries and medications. However, it has been found that progressive GON is still present in some patients with effective IOP decrease. Therefore, risk factors other than IOP elevation, like neurotrophin deprivation and excitotoxicity, contribute to progressive GON. Novel approaches of neuroprotection may be more effective for preserving the function of the optic nerve.

No MeSH data available.


Related in: MedlinePlus

Molecular mechanisms of apoptotic cell death.Notes: There are two major pathways, extrinsic and intrinsic, that are responsible for apoptotic cell death. The extrinsic pathway is initiated by binding between death ligand and death receptor, while the intrinsic pathway is initiated by efflux of cytochrome c from mitochondria. The activation of these two apoptotic pathways leads to activation of downstream effectors of apoptosis caspases 3, 6, and 7.Abbreviation: Smac, second mitochondria-derived activator of caspases.
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f4-dddt-9-1469: Molecular mechanisms of apoptotic cell death.Notes: There are two major pathways, extrinsic and intrinsic, that are responsible for apoptotic cell death. The extrinsic pathway is initiated by binding between death ligand and death receptor, while the intrinsic pathway is initiated by efflux of cytochrome c from mitochondria. The activation of these two apoptotic pathways leads to activation of downstream effectors of apoptosis caspases 3, 6, and 7.Abbreviation: Smac, second mitochondria-derived activator of caspases.

Mentions: Apoptosis is the process of programmed cell death that occurs in multicellular organisms. The extrinsic pathway is mediated by Fas receptor or tumor necrosis factor receptor (TNFR), while the intrinsic pathway is initiated by efflux of cytochrome c from mitochondria. The initiation of these two apoptotic pathways leads to activation of downstream effectors caspases 3, 6, and 7, which proteolytically degrade a host of intracellular proteins to carry out the cell death program (Figure 4). The anti-apoptotic Bcl-2 proteins, including Bcl-2 and Bcl-xl, act by directly inhibiting mitochondrial apoptosis-induced channel formation.42 By using the terminal deoxynucleotidyl transferase dUTP nick end labeling method, Quigley et al confirmed that GON was partially caused by apoptosis of RGCs in experimental glaucoma;43 Kerrigan et al confirmed that this was also the case in glaucoma patients.44 Based on these observations, anti-apoptotic agents may preserve the optic nerve structurally and functionally in glaucoma.


Neuroprotective therapies for glaucoma.

Song W, Huang P, Zhang C - Drug Des Devel Ther (2015)

Molecular mechanisms of apoptotic cell death.Notes: There are two major pathways, extrinsic and intrinsic, that are responsible for apoptotic cell death. The extrinsic pathway is initiated by binding between death ligand and death receptor, while the intrinsic pathway is initiated by efflux of cytochrome c from mitochondria. The activation of these two apoptotic pathways leads to activation of downstream effectors of apoptosis caspases 3, 6, and 7.Abbreviation: Smac, second mitochondria-derived activator of caspases.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4362661&req=5

f4-dddt-9-1469: Molecular mechanisms of apoptotic cell death.Notes: There are two major pathways, extrinsic and intrinsic, that are responsible for apoptotic cell death. The extrinsic pathway is initiated by binding between death ligand and death receptor, while the intrinsic pathway is initiated by efflux of cytochrome c from mitochondria. The activation of these two apoptotic pathways leads to activation of downstream effectors of apoptosis caspases 3, 6, and 7.Abbreviation: Smac, second mitochondria-derived activator of caspases.
Mentions: Apoptosis is the process of programmed cell death that occurs in multicellular organisms. The extrinsic pathway is mediated by Fas receptor or tumor necrosis factor receptor (TNFR), while the intrinsic pathway is initiated by efflux of cytochrome c from mitochondria. The initiation of these two apoptotic pathways leads to activation of downstream effectors caspases 3, 6, and 7, which proteolytically degrade a host of intracellular proteins to carry out the cell death program (Figure 4). The anti-apoptotic Bcl-2 proteins, including Bcl-2 and Bcl-xl, act by directly inhibiting mitochondrial apoptosis-induced channel formation.42 By using the terminal deoxynucleotidyl transferase dUTP nick end labeling method, Quigley et al confirmed that GON was partially caused by apoptosis of RGCs in experimental glaucoma;43 Kerrigan et al confirmed that this was also the case in glaucoma patients.44 Based on these observations, anti-apoptotic agents may preserve the optic nerve structurally and functionally in glaucoma.

Bottom Line: However, it has been found that progressive GON is still present in some patients with effective IOP decrease.Therefore, risk factors other than IOP elevation, like neurotrophin deprivation and excitotoxicity, contribute to progressive GON.Novel approaches of neuroprotection may be more effective for preserving the function of the optic nerve.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Peking University Third Hospital, Beijing, People's Republic of China.

ABSTRACT
Glaucoma is the second leading cause for blindness worldwide. It is mainly caused by glaucomatous optic neuropathy (GON) characterized by retinal ganglion cell loss, which leads to visual field defect and blindness. Up to now, the main purpose of antiglaucomatous therapies has been to lower intraocular pressure (IOP) through surgeries and medications. However, it has been found that progressive GON is still present in some patients with effective IOP decrease. Therefore, risk factors other than IOP elevation, like neurotrophin deprivation and excitotoxicity, contribute to progressive GON. Novel approaches of neuroprotection may be more effective for preserving the function of the optic nerve.

No MeSH data available.


Related in: MedlinePlus