摘要:
The present invention provides a method for lowering intraocular pressure and providing neuroprotection to a patient in need thereof by administering a therapeutically effective amount of at least one non-nucleotide or non-protein agent that inhibits expression and/or signaling of connective tissue growth factor (CTGF).
摘要:
Compositions containing inhibitors of cathepsin K (CTSK) expression and/or activity are provided. Methods for the treatment of glaucoma using the compositions of the invention are further provided.
摘要:
The present invention provides a method for lowering intraocular pressure and providing neuroprotection to a patient in need thereof by administering a therapeutically effective amount of at least one agent that inhibits binding and/or signaling of connective tissue growth factor (CTGF) via the TrkA/p75NTR receptor complex.
摘要:
The short form version of c-Maf transcription factor is up-regulated in steroid-treated and transforming growth factor beta2-treated trabecular meshwork cells, and is present at elevated levels in glaucomatous versus normal trabecular meshwork cells and in glaucomatous versus normal optic nerve head tissue. Expression of short form c-Maf transcription factor under these conditions indicates a causal or effector role for the factor in primary open-angle and steroid-induced glaucoma pathogenesis. Antagonism of short form c-Maf transcription factor expression and/or activity in the trabecular meshwork or other ocular tissue is provided for inhibiting or alleviating glaucoma pathogenesis. Antagonists include cyclin-dependent kinase 2 inhibitors.
摘要:
The present invention provides methods for identifying a patient at risk for developing AMD by identifying the presence of the Y402H polymorphism or other at risk variants in the complement factor H gene. The present invention further provides methods for treating persons having AMD or at risk for developing AMD as a result of having the Y402H polymorphism or other at risk variants in the complement factor H gene.
摘要:
RNA interference is provided for inhibition of ocular hypertension target mRNA expression for lowering elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension. Ocular hypertension targets include carbonic anhydrase II, IV, and XII; β1- and β2 adrenergic receptors; acetylcholinesterase; Na+/K+-ATPase; and Na—K-2Cl cotransporter. Ocular hypertension is treated by administering interfering RNAs of the present invention.
摘要翻译:提供RNA干扰用于抑制眼高血压靶mRNA表达,以降低开角型青光眼或高眼压患者眼内压升高。 眼睛高血压指标包括碳酸酐酶II,IV和XII; β1-和β2肾上腺素能受体; 乙酰胆碱酯酶; Na + + / K + + -ATP酶; 和Na-K-2Cl共转运蛋白。 通过施用本发明的干扰RNA来治疗眼高血压。
摘要:
The present invention provides a method for lowering intraocular pressure and providing neuroprotection to a patient in need thereof by administering a therapeutically effective amount of at least one non-nucleotide or non-protein agent that inhibits expression and/or signaling of lysyl oxidase (LOX) or a lysyl oxidase-like protease (LOXL).
摘要:
RNA interference is provided for inhibition of ocular hypertension target mRNA expression for lowering elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension. Ocular hypertension targets include carbonic anhydrase II, IV, and XII; β1- and β2 adrenergic receptors; acetylcholinesterase; Na+/K+-ATPase; and Na—K-2Cl cotransporter. Ocular hypertension is treated by administering interfering RNAs of the present invention.
摘要翻译:提供RNA干扰用于抑制眼高血压靶mRNA表达,以降低开角型青光眼或高眼压患者眼内压升高。 眼睛高血压指标包括碳酸酐酶II,IV和XII; β1-和β2肾上腺素能受体; 乙酰胆碱酯酶; Na + + / K + + -ATP酶; 和Na-K-2Cl共转运蛋白。 通过施用本发明的干扰RNA来治疗眼高血压。
摘要:
The invention provides pharmaceutical compositions containing non-feminizing estrogen and methods of using these compositions to prevent or ameliorate retinal and optic nerve damage associated with glaucoma.
摘要:
The present invention provides compositions and methods for treating glaucoma, methods for diagnosing glaucoma, and methods for identifying agents which may be useful in the treatment of glaucoma. More specifically, the present invention describes the use of agents that modulate the expression of serum amyloid A.