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Posted On: 12/03/2024 4:34:20 PM
Post# of 148870
Glaucoma and the CCR5 connection.
Excerpt: "The CCR5-CCL5 antibody effectively prolonged filtration bleb duration and enhanced the functionality of the filtered bleb. Improved postoperative intraocular pressure values (IOP) and morphological images were observed in the CCR5-CCL5 antibody-treated group. Histochemical staining and cellular experiments confirmed the antifibrotic function of the CCR5-CCL5 antibody. Notably, M2-type macrophage polarization was reduced in the CCR5-CCL5 antibody-treated model. CCL5-induced fibrosis in HConFs was mediated through the PI3K/Akt signaling pathway. Consistently, inhibition of PI3K/Akt significantly attenuated the profibrotic effects of CCR5-CCL5. Mechanistically, the CCL5 antibody exerts its antifibrotic effect by targeting CCR5 on HConFs, leading to the inhibition of the PI3K/Akt mechanism."
https://pubmed.ncbi.nlm.nih.gov/39618346/
Credit Bluemoon on IVillage
Excerpt: "The CCR5-CCL5 antibody effectively prolonged filtration bleb duration and enhanced the functionality of the filtered bleb. Improved postoperative intraocular pressure values (IOP) and morphological images were observed in the CCR5-CCL5 antibody-treated group. Histochemical staining and cellular experiments confirmed the antifibrotic function of the CCR5-CCL5 antibody. Notably, M2-type macrophage polarization was reduced in the CCR5-CCL5 antibody-treated model. CCL5-induced fibrosis in HConFs was mediated through the PI3K/Akt signaling pathway. Consistently, inhibition of PI3K/Akt significantly attenuated the profibrotic effects of CCR5-CCL5. Mechanistically, the CCL5 antibody exerts its antifibrotic effect by targeting CCR5 on HConFs, leading to the inhibition of the PI3K/Akt mechanism."
https://pubmed.ncbi.nlm.nih.gov/39618346/
Credit Bluemoon on IVillage
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