This condition is characterized by the progressive apoptosis of retinal ganglion cells (RGCs), a type of neuron vital for transmitting visual information from the eye to the brain. The primary culprit behind glaucomatous optic neuropathy, the hallmark of the disease, is elevated intraocular pressure.
Current treatments primarily revolve around reducing intraocular pressure through medications or surgical interventions. While these approaches have proven effective in managing glaucoma to some extent, they fall short of preventing the relentless degeneration of RGCs and their axons, highlighting the pressing need for novel therapeutic strategies.
The Enigmatic World of MicroRNAs
MicroRNAs (miRNAs) are small, non-coding RNA molecules, typically around 22 nucleotides in length, that play a pivotal role in regulating gene expression at the post-transcriptional and translational levels. These endogenous molecules are widespread in biological genomes and have only come to light in recent years.
MiRNAs govern a multitude of physiological and pathological processes, including cell proliferation, apoptosis, differentiation, and organogenesis. As such, they have garnered significant attention in the context of glaucoma research, with the hope of unlocking their therapeutic potential.
The Role of miRNAs in Glaucoma
MiR-93 as a Potential Game Changer
One such miRNA that has surfaced as a potential game-changer in the battle against glaucoma is miR-93. A study led by Wang et al. demonstrated that miR-93 plays a significant role in promoting apoptosis in glaucomatous trabecular meshwork (TM) cells. By transfecting TM cells with lentiviruses containing specific inhibitors of miR-93, they managed to suppress miR-93 expression and observed a substantial increase in TM cell viability. This finding suggests that miR-93 may hold promise as a therapeutic target for glaucoma, given its role in promoting cell death.
The Missing Piece: RGC Apoptosis and miR-93
While miR-93’s impact on TM cells has been studied, the question of whether it influences RGC apoptosis and its role in glaucoma animal models remains shrouded in mystery. Understanding this aspect of miR-93’s function is crucial to elucidate its potential in glaucoma therapy.
To address this gap in knowledge, the aim of the current study is to unravel the role of miR-93 in promoting RGC apoptosis and retinal damage in mice afflicted with acute glaucoma. Furthermore, the study seeks to delve into the molecular mechanisms underlying miR-93’s actions in the context of glaucomatous retinal damage.
The Path Forward
The research into miR-93’s role in glaucoma therapy presents an exciting avenue for potential treatment breakthroughs. By elucidating its impact on RGCs and its function in glaucoma animal models, we may uncover a powerful tool in our arsenal against this insidious blinding disease.
It is important to note that the current state of research on miRNAs in glaucoma, including miR-93, is still in its infancy, and persuasive clinical evidence is lacking. Nevertheless, the growing interest in miRNAs as specific drug targets for the diagnosis and treatment of glaucoma is a testament to the urgency and importance of finding more effective therapies.
In conclusion, glaucoma remains a leading cause of blindness worldwide, primarily due to the apoptosis of retinal ganglion cells driven by elevated intraocular pressure. Current treatments, while effective to a certain extent, do not entirely prevent the degeneration of these crucial cells.
The potential of miRNAs, such as miR-93, in preserving RGCs and vision offers hope for a brighter future for glaucoma patients. The ongoing research endeavors to decipher miR-93’s role in RGC apoptosis and its function in glaucoma animal models hold the promise of innovative treatments that could revolutionize the management of this debilitating eye disease. While the journey to conclusive clinical evidence is still ongoing, the pursuit of miRNA-based glaucoma therapies is a beacon of hope for millions affected by this silent thief of sight.
reference link : https://www.cell.com/heliyon/fulltext/S2405-8440(23)09220-4