Nikhil Prasad Fact checked by:Thailand Medical News Team Aug 10, 2026 1 hour, 55 minutes ago
Glaucoma is widely associated with increased pressure inside the eye, but scientists are increasingly finding that the disease involves far more than eye pressure alone. A detailed scientific review has highlighted how two important retinal cell types—astrocytes and Müller glia cells—can undergo major changes that may accelerate inflammation, nerve damage and glaucoma progression.
Astrocytes and Müller glia cells can shift from protecting the retina to promoting inflammation and
neurodegeneration during glaucoma progression
These cells normally protect the retina and help keep its delicate environment functioning properly. However, prolonged mechanical, metabolic and inflammatory stress can transform them from neuroprotective cells into active contributors to retinal neurodegeneration.
Researchers Examine Glial Cells in Glaucoma
The review was undertaken by researchers from the Laboratory of Retinal Neurobiology, Department of Neurobiology, Institute of Biology, Fluminense Federal University; Graduate Program of Neurosciences, Institute of Biology, Fluminense Federal University; Graduate Program of Biomedical Sciences, Biomedical Institute, Fluminense Federal University; and Laboratory of Neuronal Physiology and Pathology, Department of Molecular and Cellular Biology, Institute of Biology, Fluminense Federal University, Brazil.
The researchers stressed that glaucoma can continue progressing despite adequate control of intraocular pressure. This suggests that pressure-independent mechanisms—including oxidative stress, mitochondrial dysfunction and neuroinflammation—can continue damaging retinal ganglion cells, whose axons form the optic nerve.
Astrocytes Can Change from Protective to Neurotoxic
Healthy astrocytes provide metabolic assistance, regulate the retinal environment and protect retinal ganglion cell axons. During glaucoma, mechanical stress can activate channels including PIEZO1 and TRP channels, triggering cellular responses to pressure and tissue deformation.
Initially, these responses can be protective. With persistent stress, however, astrocytes can undergo oxidative damage and cellular senescence. They may begin producing inflammatory and tissue-remodeling molecules while activating pathways involving CXCL10, complement C3, NF-κB and the NLRP3 inflammasome.
The resulting environment can accelerate retinal ganglion cell injury. Importantly, this inflammatory activity may become self-sustaining and potentially continue even after intraocular pressure has been successfully reduced.
Müller Glia Cells Also Undergo a Dangerous Transformation
This Thailand
Medical News report highlights how Müller glia cells, which extend across the entire retinal thickness, are equally important. Normally, they regulate potassium and water, remove excess glutamate, provide antioxidants and release neuroprotective factors.
Early activation can actually strengthen these protective functions. Pro
longed glaucoma-related stress, however, can reduce important proteins involved in potassium regulation and glutamate handling.
The resulting accumulation of extracellular glutamate can excessively stimulate NMDA receptors on retinal ganglion cells. This causes calcium overload, mitochondrial dysfunction, increased production of damaging reactive oxygen species and ultimately greater neuronal death.
Mechanosensitive channels including TRPV4 and PIEZO1, together with oxidative-stress-sensitive TRPA1, may further amplify Müller glial dysfunction, inflammation and metabolic failure.
An Interconnected Neuroinflammatory Network
Another important finding is that astrocytes and Müller glia do not operate independently. They communicate with microglia and retinal ganglion cells through inflammatory molecules, ATP, complement proteins and other signaling systems.
This creates the possibility of a vicious cycle in which stressed retinal cells activate glia, activated glia increase inflammation, and inflammatory signals cause additional neuronal injury. Such interconnected signaling could help explain why glaucoma sometimes worsens despite normalized eye pressure.
New Therapeutic Strategies Could Target Glial Dysfunction
The researchers propose that future treatments should not completely suppress glial activation because early responses can be protective. Instead, therapies may need to prevent the transition toward chronic neurotoxic activity.
Potential approaches include targeting TRP channels, oxidative stress, complement signaling, NF-κB and NLRP3. Gene therapies delivering neuroprotective factors such as BDNF, CNTF and GDNF, or strengthening antioxidant pathways such as SOD2, are also being investigated conceptually and preclinically.
Conclusions
The review shows that astrocytes and Müller glia cells are active participants in glaucoma progression rather than simply responding to existing retinal damage. Understanding exactly when these cells switch from neuroprotective to neurotoxic states could lead to treatments that preserve their beneficial functions while stopping chronic inflammation, oxidative injury and irreversible retinal ganglion cell loss.
The study findings were published in the peer reviewed International Journal of Molecular Sciences.
https://www.mdpi.com/1422-0067/27/15/6895
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