Glaucoma: From Molecular Mechanisms to Innovative Therapeutics
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: 31 August 2026 | Viewed by 197
Editor
Interests: ophthalmology; eye diseases; neuroprotection
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Glaucoma represents a heterogeneous group of optic neuropathies characterized by the progressive degeneration of retinal ganglion cells (RGCs) and irreversible visual field loss. As the leading cause of irreversible blindness globally, it poses a profound public health challenge. Current epidemiological data suggests that the burden of glaucoma is rising; with a rapidly aging global population, the number of affected individuals is projected to exceed 111 million by the year 2040.
Traditionally, the management of glaucoma has been singular in its focus: the reduction of intraocular pressure (IOP). Elevated IOP remains the only proven modifiable risk factor for the development and progression of the disease. Consequently, the standard of care—ranging from topical hypotensive agents and laser trabeculoplasty to filtration surgeries—targets the IOP dynamics of the anterior segment to facilitate aqueous humor outflow. While these interventions are effective for many, they are not curative. A significant subset of patients continues to experience visual deterioration despite achieving target IOP levels, a phenomenon notably prevalent in normal-tension glaucoma. This clinical paradox highlights a critical gap in our understanding: lowering pressure is often necessary, but it is not always sufficient to halt neurodegeneration.
This limitation has catalyzed a paradigm shift in glaucoma research, moving beyond the "IOP" view of the disease toward a "neurodegenerative" perspective. Recent advances have begun to unravel the complex molecular machinery driving RGC death, implicating mechanisms such as oxidative stress, mitochondrial dysfunction, excitotoxicity, neuroinflammation, and cytoskeletal defects in the trabecular meshwork. Understanding these molecular underpinnings is no longer just an academic exercise; it is the foundation for the next generation of treatments.
This Special Issue aims to bridge the gap between these fundamental molecular discoveries and emerging clinical applications. We will examine the pathophysiology of glaucoma through a molecular lens, exploring how dysfunction in pathways such as Rho kinase (ROCK) signaling and nitric oxide (NO) regulation has led to the first new class of glaucoma drugs in decades. Furthermore, we will explore the frontier of "innovative therapeutics," including neuroprotective strategies, gene therapies targeting specific mutations (such as MYOC and OPTN), and the potential of regenerative medicine. By connecting molecular mechanisms to therapeutic innovation, we can envision a future where glaucoma management evolves from delaying blindness to preserving and potentially restoring vision.
Prof. Dr. Da-Wen Lu
Guest Editor
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Keywords
- neuroprotection
- reinal ganglion cell
- therapeutic strategies
- Rho kinase inhibitor
- molecular research
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