Primary open-angle glaucoma (POAG) is a common form of glaucoma in which retinal ganglion cells (RGCs) die at varying intervals. Primary open-angle glaucoma is often associated with an increased intraocular pressure (IOP), which when reduced, can slow down the progression of the disease. However, it is essential to develop better modes of treatments for glaucoma patients. In this overview, we discuss the hypothesis that RGC mitochondria are affected during the initiation of POAG, by becoming gradually weakened, but at different rates because of their specific receptor profiles. With this in mind, we argue that neuroprotection in the context of glaucoma should focus on preserving RGC mitochondrial function and suggest a number of ways by which this can theoretically be achieved. Since POAG is a chronic disease, any neuroprotective treatment strategy must be tolerated over many years. Theoretically, topically applied substances should have the fewest side effects, but it is questionable whether sufficient compounds can reach RGC mitochondria to be effective. Therefore, other delivery procedures that might result in greater concentrations of neuroprotectants reaching RGC mitochondria are being developed. Red-light therapy represents another therapeutic alternative for enhancing RGC mitochondrial functions and has the advantage of being both non-toxic and non-invasive.
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http://dx.doi.org/10.1016/j.ejphar.2016.04.032 | DOI Listing |
Medicine (Baltimore)
January 2025
Opthalmology, Chongqing Hechuan District People's Hospital, Chongqing, China.
Background: Bushen-Huoxue-Mingmu-Formula (MMF) has achieved definite clinical efficacy. However, its mechanism is still unclear.
Objective: Investigating the molecular mechanism of MMF to protect retinal ganglion cells (RGCs).
Exp Eye Res
December 2024
Department of Ophthalmology & Visual Science, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, 200031, China; State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, 200032, China; NHC Key Laboratory of Myopia, Chinese Academy of Medical Sciences, And Shanghai Key Laboratory of Visual Impairment and Restoration (Fudan University), Shanghai, 200031, China. Electronic address:
We aimed to explore the protective effects and underlying mechanisms of taurine on retinal cells during acute ocular hypertension (AOH)-induced damage. Retinal morphology, apoptosis, mitochondrial structure, electroretinography, expression of GTP binding protein 3 (GTPBP3), and molecules in the unfolded protein response (UPR) were examined in an AOH mouse model and wild-type (WT) mice with or without intravitreal injection of taurine. For in vitro experiments, the GTPBP3 expression and endoplasmic reticulum (ER) stress were examined in R28 cell line under hydrogen peroxide (HO)-induced damage or hypoxia/reoxygenation (H/R)-induced damage, with or without taurine pretreatment.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Pharmacology and Neuroscience, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Glaucoma is a heterogenous group of optic neuropathies characterized by the degeneration of optic nerve axons and the progressive loss of retinal ganglion cells (RGCs), which could ultimately lead to vision loss. Elevated intraocular pressure (IOP) is a major risk factor in the development of glaucoma, and reducing IOP remains the main therapeutic strategy. Endothelin-1 (ET-1), a potent vasoactive peptide, has been shown to produce neurodegenerative effects in animal models of glaucoma.
View Article and Find Full Text PDFAdv Healthc Mater
December 2024
Shenzhen Key Laboratory of Marine Biomedical Materials, CAS-HK Joint Lab of Biomaterials, The Key Laboratory of Biomedical Imaging Science and System, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, P.R. China.
Tumor therapy has advanced significantly in recent years, but tumor cells can still evade and survive the treatment through various mechanisms. Notably, tumor cells use autophagy to sustain viability by removing impaired mitochondria and clearing excess reactive oxygen species (ROS). In this study, the aim is to amplify intracellular oxidative stress by inhibiting mitochondrial autophagic flux.
View Article and Find Full Text PDFJCI Insight
November 2024
Center for Mitochondrial Biomedicine and Department of Ophthalmology, the Fourth Affiliated Hospital.
The degeneration of retinal ganglion cells (RGC) due to mitochondrial dysfunctions manifests optic neuropathy. However, the molecular components of RGC linked to optic neuropathy manifestations remain largely unknown. Here, we identified a potentially novel optic atrophy-causative CRYAB gene encoding a highly conserved major lens protein acting as mitochondrial chaperone and possessing antiapoptotic activities.
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