Macular Hole and Netra Restoration Therapy

A Comprehensive Therapy Designed to Support the Key Underlying Drivers of Macular Hole

A macular hole is a defect in the central macula, the part of the retina responsible for reading, recognizing faces, seeing fine detail, and performing visually demanding tasks. Some macular holes are partial thickness, some are lamellar, and some are full thickness, meaning the defect extends through the neurosensory retina at the fovea. The International Vitreomacular Traction Study Group defined a full-thickness macular hole as a foveal lesion with interruption of all retinal layers from the internal limiting membrane to the retinal pigment epithelium and classified holes by size, cause, and the presence or absence of vitreomacular traction.

For many patients, the diagnosis feels purely structural: there is a hole in the macula. Structurally, that is true. But the biological story is broader. Macular hole formation often involves abnormal vitreomacular interface forces, tangential traction, foveal tissue stretching, intraretinal cystic change, photoreceptor stress, Müller cell response, glial remodeling, and disruption of outer retinal structures such as the external limiting membrane and ellipsoid zone. These are not isolated events. They occur within living retinal tissue that depends on oxygen delivery, mitochondrial energy, microvascular regulation, inflammatory balance, neurotrophic signaling, and cellular repair capacity.

Netra Restoration Therapy, or NRT, is a full-spectrum integrative ophthalmology platform designed to support the biological terrain that influences retinal and macular health. For macular hole, NRT should be understood with careful scientific precision. NRT is not presented as a mechanical closure procedure for a full-thickness macular hole. It is not a substitute for retinal imaging, ophthalmic monitoring, or urgent evaluation when central vision changes suddenly. Its role is supportive and adjunctive: to help optimize the retinal environment in which macular tissue functions, responds to stress, and maintains cellular resilience.

This distinction matters. A macular hole has a mechanical and anatomical component. At the same time, the function of the macula depends on more than anatomy alone. Visual outcome is influenced by photoreceptor integrity, foveal architecture, glial support, retinal fluid regulation, mitochondrial health, and the condition of surrounding retinal tissue. OCT studies repeatedly show that outer retinal biomarkers such as the external limiting membrane and ellipsoid zone are important indicators of visual potential. This supports the integrative concept that protecting the tissue around the hole and supporting the remaining viable retina may be meaningful.

For macular hole, NRT is designed to support several interconnected biological priorities:

• Retinal and choroidal microcirculation that supports oxygen and nutrient delivery to macular tissue.
• Inflammatory balance around the retina and vitreomacular interface.
• Oxidative stress reduction to protect photoreceptors, Müller cells, and retinal pigment epithelium.
• Mitochondrial function in photoreceptors and retinal support cells.
• Neuroprotection and neurotrophin activity, including pathways involving BDNF and NGF.
• Müller cell and glial support, which are central to retinal structure, water balance, neurotransmitter clearance, and tissue remodeling.
• Retinal fluid regulation and tissue hydration balance.
• Whole-person factors such as metabolic health, sleep, stress physiology, inflammation, and vascular regulation.

The purpose of a multi-target NRT approach is not to claim that every macular hole can be reversed through integrative care. The purpose is to address the broader biological environment that can influence retinal resilience, visual function, tissue stress, and recovery terrain. In this way, NRT fits within a full-spectrum model of integrative ophthalmology: one that respects structural diagnosis while also asking what biological factors may be weakening the macula, impairing repair capacity, or limiting functional recovery.

Why Treatment for Macular Hole Should Be Multi-Factorial

Macular hole should be approached as a multifactorial condition because the fovea is not simply a passive sheet of tissue. It is a highly specialized region of neural retina with delicate structural architecture, dense photoreceptor specialization, unique glial organization, and high metabolic demand. A visible hole may form because of mechanical traction, but the tissue response to that traction depends on cellular health, retinal fluid handling, extracellular matrix behavior, mitochondrial energy, oxidative stress, and neurovascular support.

A purely structural explanation is useful but incomplete. The question is not only, 'Is there a hole?' The broader questions are: why did the foveal tissue become vulnerable? Is there vitreomacular traction? Is there tangential traction from an epiretinal membrane? Are there cystoid spaces around the hole? Are the photoreceptors disrupted? Is the ellipsoid zone damaged? Is there coexisting myopia, trauma, diabetic retinal disease, inflammation, or retinal degeneration? These questions make macular hole care inherently multi-factorial.

Vitreomacular Interface Stress

The most recognized driver of idiopathic macular hole is abnormal interaction between the posterior vitreous and the macula. During aging, the vitreous may detach from the retina. If detachment is incomplete and the vitreous remains abnormally adherent to the fovea, tractional forces can distort the central macula. These forces may be anteroposterior, tangential, or both. Over time, traction can produce foveal dehiscence, cystoid spaces, photoreceptor disruption, and a partial- or full-thickness defect.

NRT does not remove traction mechanically. However, an integrative approach can still be relevant to the biological terrain surrounding vitreomacular interface disease. The macula experiencing traction is living tissue. It must regulate inflammation, fluid balance, oxidative stress, mitochondrial energy, and glial response. Supporting these pathways may help protect the surrounding retina and improve the quality of the retinal environment.

Foveal Tissue Vulnerability

The fovea is anatomically thin and highly specialized. It lacks the same structural redundancy found in other retinal regions. Involutional foveal thinning, aging-related vitreous change, myopic stretching, trauma, or pre-existing macular disease can increase vulnerability. Once foveal tissue is under tractional stress, weak cellular resilience may make the tissue less able to maintain integrity.

This is where a systems-based model becomes important. Retinal tissue vulnerability may be influenced by oxidative stress, impaired perfusion, mitochondrial dysfunction, chronic inflammation, glycemic stress, nutritional insufficiency, sleep quality, and systemic vascular health. NRT seeks to address these broader factors instead of looking at the hole as a single isolated event.

Photoreceptor and Outer Retinal Integrity

The visual impact of a macular hole is closely related to the condition of the photoreceptors around the fovea. OCT biomarkers such as the external limiting membrane and ellipsoid zone are often used to interpret outer retinal integrity. The ellipsoid zone reflects the inner segment region of photoreceptors and is closely linked to mitochondrial density and photoreceptor function. When this region is disrupted, visual recovery potential may be limited even when the anatomy appears improved.

NRT therefore emphasizes photoreceptor resilience. Supporting oxygen delivery, mitochondrial function, antioxidant defenses, neurotrophic signaling, and inflammatory balance may help optimize the surrounding retinal tissue. This is supportive care, not a claim of guaranteed closure.

Müller Cell and Glial Response

Müller cells are the principal glial cells of the retina. They span the retinal thickness and help regulate retinal structure, potassium balance, water movement, neurotransmitter clearance, metabolic support, and tissue repair. In macular hole biology, Müller cells are especially important because foveal architecture depends heavily on glial support. Research on spontaneous closure of small full-thickness macular holes has described bridging phenomena involving Müller cell-related tissue responses.

The NRT model gives attention to glial health because a stressed retina is not only a neuronal tissue; it is a neuro-glial-vascular unit. Supporting Müller cell function means supporting the retina's ability to regulate fluid, neurotransmitters, inflammation, and structural stability.

Inflammation, Oxidative Stress, and Tissue Remodeling

Macular hole is not generally categorized as a primary inflammatory disease. Still, inflammation and oxidative stress can influence the health of retinal cells surrounding the hole. Chronic oxidative stress can weaken photoreceptors, impair mitochondrial function, activate microglia, and reduce cellular repair capacity. Inflammation can also influence glial activation and extracellular matrix remodeling at the vitreoretinal interface.

A multi-factorial approach therefore includes reducing systemic and retinal stressors that may impair tissue resilience. NRT addresses inflammation and oxidative burden through nutrition, botanical support, acupuncture-based neurovascular regulation, metabolic support, sleep and stress physiology, and whole-person care.

Systemic and Whole-Person Factors

Although macular hole is localized to the eye, the biological condition of the retina is influenced by the whole body. Vascular health, metabolic status, inflammatory load, oxidative burden, hydration, sleep quality, stress physiology, and nutritional status can shape retinal resilience. Patients with high myopia, diabetes, inflammatory disorders, chronic stress, or poor circulation may have additional biological challenges that affect macular tissue.

A multi-factorial strategy does not replace structural eye care. It expands the clinical lens. NRT asks what can be done to support the tissue environment around the macula, improve the patient's systemic terrain, and protect remaining visual function.

Key Biological Mechanisms in Macular Hole

Vitreomacular Traction

Vitreomacular traction is one of the central mechanisms in macular hole formation. Incomplete posterior vitreous detachment may leave the posterior hyaloid attached to the fovea. When the vitreous pulls on the macula, it can distort the foveal contour and create intraretinal stress. Over time, this may lead to cystic spaces, foveal splitting, and full-thickness tissue disruption.

The International Vitreomacular Traction Study Group classification helped standardize how clinicians describe vitreomacular adhesion, vitreomacular traction, and macular holes using OCT. This classification emphasizes the importance of structural traction, hole size, primary versus secondary cause, and the presence or absence of ongoing vitreomacular traction.

Tangential Traction and Epiretinal Interface Stress

Not all macular traction is vertical. Tangential forces can arise from epiretinal membrane, internal limiting membrane stiffness, fibrocellular proliferation, or vitreoschisis. These tangential forces may flatten, stretch, or distort the fovea. In some eyes, tractional stress creates a pseudohole or lamellar hole; in others, it contributes to a full-thickness defect.

From an integrative perspective, interface stress is not purely mechanical. Fibrocellular proliferation and extracellular matrix remodeling are influenced by cellular signaling, inflammation, glial activation, and tissue repair pathways. NRT does not remove membranes, but it can support a healthier retinal environment by addressing inflammatory and oxidative terrain.

Foveal Cystic Change and Retinal Fluid Imbalance

Cystoid spaces are frequently seen around macular holes on OCT. These spaces may reflect traction-induced separation of retinal layers, Müller cell stress, and impaired retinal fluid regulation. Müller cells are critical for water and ion homeostasis in the retina. When they are stressed, fluid handling and retinal architecture can be compromised.

NRT supports retinal fluid terrain by focusing on microcirculation, inflammatory balance, glial function, metabolic health, and tissue hydration regulation. This is especially relevant when macular hole coexists with edema-like changes, retinal vascular disease, inflammation, or metabolic stress.

Müller Cell Dysfunction and Glial Remodeling

Müller cells provide structural and metabolic support to retinal neurons. They help clear extracellular glutamate, regulate potassium and water movement, maintain the retinal extracellular environment, interact with retinal blood vessels, and support photoreceptor function. In macular hole, glial remodeling may be part of both tissue injury and tissue response.

The role of Müller cells is especially important because visual recovery depends not only on anatomical closure but also on restoration of retinal microstructure. Glial tissue may help bridge defects in certain small holes, but excessive or maladaptive gliosis may also contribute to distortion and scarring. NRT seeks to support healthy glial function rather than force a simplistic pro- or anti-gliosis response.

Photoreceptor Disruption

A macular hole affects central vision because it disrupts the foveal photoreceptor architecture. Photoreceptor integrity is often assessed on OCT by reviewing the external limiting membrane, ellipsoid zone, and interdigitation zone. These layers provide clues about whether photoreceptor structure remains viable.

Photoreceptors are energy-intensive cells. Their inner segments contain mitochondria that support visual function. When oxidative stress, mitochondrial dysfunction, hypoxia, or inflammation are present, photoreceptors may be less resilient. NRT places strong emphasis on photoreceptor protection and mitochondrial support.

Mitochondrial Dysfunction

The macula requires high energy production. Photoreceptors, Müller cells, and retinal pigment epithelial cells depend on mitochondria for ATP production, calcium signaling, redox balance, and cell survival. Mitochondrial dysfunction can increase oxidative stress, impair repair capacity, and contribute to neurodegeneration.

In macular hole, mitochondrial support is relevant because visual function depends on the tissue surrounding the hole. Even when the structural defect is visible, the remaining retinal cells must continue functioning. NRT supports mitochondrial resilience through nutrition, blood flow, oxygen delivery, metabolic support, sleep, stress regulation, and botanical compounds with antioxidant and mitochondrial relevance.

Oxidative Stress

The retina is vulnerable to oxidative stress because it has high oxygen consumption, intense light exposure, and lipid-rich membranes. Oxidative stress can injure photoreceptors, retinal pigment epithelial cells, mitochondria, and glial cells. Although macular hole is not primarily an oxidative disease, oxidative burden may reduce the resilience of the retinal tissue around the hole.

NRT addresses oxidative stress as a general retinal vulnerability factor. The objective is not to claim that antioxidants close a macular hole. The objective is to reduce cellular stress and support healthier retinal biology.

Inflammatory Signaling and Microglial Activation

Retinal inflammation can involve microglia, cytokines, complement-related activity, and glial signaling. In macular hole, inflammatory signaling may be secondary to tissue stress, traction, retinal injury, or coexisting retinal conditions. Cytokines can influence extracellular matrix remodeling, vascular permeability, oxidative stress, and glial response.

NRT seeks to support inflammatory balance through a whole-person approach. This includes addressing diet, gut-retina signaling, metabolic inflammation, stress physiology, sleep quality, and botanical or acupuncture-based modulation of inflammatory pathways when appropriate.

Neurotrophin Biology: BDNF and NGF

The retina is part of the central nervous system. Neurotrophins such as BDNF and NGF support neuronal survival, plasticity, repair, and resilience. Neurotrophin research is strongest in retinal neurodegeneration and optic nerve disorders, but the concept is also relevant to macular hole because the tissue around the defect contains stressed neural retina.

NRT includes neuroprotective support as a core principle. Supporting neurotrophic signaling may help create a more favorable environment for photoreceptors, retinal neurons, and glial cells. This should be described as supportive biology, not as a proven macular-hole closure therapy.

Ocular Blood Flow and Microcirculation

The macula depends on retinal and choroidal circulation for oxygen, nutrient delivery, waste removal, and metabolic stability. While traction is the central mechanical factor in many macular holes, poor perfusion can reduce tissue resilience. Microvascular health may be especially relevant in patients with diabetes, hypertension, smoking history, vascular dysregulation, sleep apnea, systemic inflammation, or high myopia.

NRT supports ocular microcirculation through integrative strategies aimed at vascular regulation, endothelial function, autonomic balance, and systemic circulatory health.

Excitotoxicity and Glutamate Handling

Müller cells help clear extracellular glutamate and maintain neurotransmitter balance in the retina. When Müller cells are stressed, glutamate handling may be impaired, increasing vulnerability to excitotoxic injury. Excitotoxicity is not usually presented as the primary cause of macular hole, but it is relevant to retinal neuroprotection and cellular stress responses.

NRT's neuroprotective framework includes support for glial health, mitochondrial function, inflammation control, and metabolic stability, all of which may influence the retina's ability to manage excitotoxic stress.

Cellular Senescence and Aging Biology

Most idiopathic macular holes occur in older adults. Aging affects the vitreous, internal limiting membrane, extracellular matrix, mitochondria, inflammatory tone, vascular regulation, and tissue repair capacity. Cellular senescence may increase inflammatory signaling and reduce regenerative capacity.

NRT evaluates macular hole within this broader aging biology. Supporting the retina means supporting the body's repair terrain, metabolic reserve, circulation, inflammatory balance, and mitochondrial function.

What Is Netra Restoration Therapy for Macular Hole?

Netra Restoration Therapy is a comprehensive, multi-target integrative ophthalmology platform designed to support ocular health through multiple biological pathways at the same time. For macular hole, NRT focuses on the biological terrain of the macula rather than claiming to mechanically close a retinal defect.

This distinction is clinically important. A full-thickness macular hole is an anatomical disruption of the foveal retina. It should be properly diagnosed and monitored with retinal examination and OCT. NRT is best described as supportive, adjunctive care that seeks to improve the health of the surrounding retina, support visual function, and address biological stressors that may influence macular resilience.

For macular hole, NRT may include individualized combinations of:

• Acupuncture-based ocular support focused on neurovascular regulation and autonomic balance.
• Traditional Chinese Medicine principles interpreted through circulation, inflammation, tissue nourishment, and retinal resilience.
• Ayurvedic medicine principles interpreted through nervous system balance, tissue nourishment, inflammatory tone, and vitality.
• Herbal and botanical support selected for antioxidant, vascular, mitochondrial, neuroprotective, and anti-inflammatory relevance.
• Nutritional strategies to support retinal metabolism, mitochondrial function, and antioxidant reserve.
• Functional medicine evaluation of systemic drivers such as inflammation, glycemic status, vascular health, gut health, sleep, and stress physiology.
• Lifestyle support for circulation, metabolic stability, sleep quality, and visual function.

NRT is individualized. A patient with a small lamellar hole, vitreomacular traction, diabetic retinal disease, high myopia, retinal thinning, or chronic inflammation may require different supportive priorities. The clinical goal is to understand the patient's retinal status and whole-body terrain, then support the pathways most relevant to that person.

NRT does not guarantee improvement and should not be used to delay urgent evaluation for new central distortion, a sudden dark spot, rapidly reduced central vision, or new metamorphopsia. The safest framing is that NRT supports retinal resilience, cellular health, and whole-person factors that influence the macular environment.

How NRT Supports the Biological Terrain in Macular Hole

Supporting Retinal and Choroidal Microcirculation

Healthy circulation is essential for retinal function. The macula requires steady oxygen delivery, nutrient exchange, and waste clearance. NRT supports ocular microcirculation through strategies aimed at vascular regulation, autonomic balance, endothelial health, and systemic circulatory support. This may be especially important in patients with vascular risk factors, diabetes, high myopia, or chronic inflammatory burden.

Supporting Photoreceptor Resilience

The visual consequences of macular hole depend heavily on the health of photoreceptors around the fovea. NRT supports photoreceptor resilience through antioxidant strategies, mitochondrial support, nutrition, blood flow support, neuroprotection, and inflammatory balance. The objective is to support the tissue that remains viable and reduce biological stress around the macula.

Supporting Müller Cell and Retinal Glial Function

Müller cells are central to retinal architecture, fluid balance, neurotransmitter clearance, and metabolic support. NRT views glial support as a major target in macular hole terrain. Supporting Müller cell function may involve reducing oxidative stress, improving metabolic stability, supporting circulation, and balancing inflammatory signaling.

Supporting Mitochondrial Function

Photoreceptor and retinal support cells are energy-demanding. Mitochondrial dysfunction can reduce retinal resilience and increase oxidative injury. NRT supports mitochondrial function through nutritional, metabolic, botanical, circulatory, and lifestyle-based strategies. This is especially relevant when OCT shows outer retinal stress or when systemic metabolic factors may impair energy production.

Supporting Oxidative Stress Reduction

Oxidative stress can damage retinal lipids, proteins, mitochondria, and DNA. Although macular hole is not primarily caused by oxidative stress, high oxidative burden may reduce the retina's ability to tolerate tractional or structural injury. NRT addresses oxidative stress through diet, botanical compounds, antioxidant reserve, inflammation reduction, sleep optimization, and metabolic support.

Supporting Inflammatory Balance

Inflammation can alter extracellular matrix behavior, glial activation, vascular permeability, and tissue repair. NRT seeks to support a balanced inflammatory response rather than suppressing normal immune function. This may include gut health support, dietary planning, stress regulation, acupuncture-based neuromodulation, and herbal strategies selected through a systems-biology lens.

Supporting Neurotrophin Activity

Neurotrophins such as BDNF and NGF support neural tissue resilience. In retinal disease research, BDNF and related pathways are studied for their role in neuronal survival, plasticity, and neuroprotection. NRT incorporates this concept by supporting neurovascular signaling, mitochondrial health, inflammation balance, and retinal cellular resilience.

Supporting Retinal Fluid and Tissue Hydration Balance

Macular holes may be surrounded by cystic or edema-like spaces, especially when traction, glial stress, or coexisting retinal disease is present. NRT supports retinal fluid terrain by addressing inflammation, vascular function, Müller cell health, systemic fluid regulation, metabolic stability, and tissue oxygenation.

Supporting the Gut-Retina and Immune-Metabolic Axis

The gut-retina axis is an emerging concept in ophthalmology. Systemic inflammation, gut barrier dysfunction, microbiome imbalance, and metabolic stress may influence retinal inflammation and vascular function. While macular hole is not caused by the gut alone, systemic inflammatory terrain can influence retinal resilience. NRT may evaluate digestion, absorption, diet, inflammatory triggers, and metabolic markers as part of whole-person macular support.

Translating TCM Concepts into Biomedical Language

Traditional Chinese Medicine may describe macular and retinal vulnerability using patterns such as Blood Stasis, Qi Deficiency, Liver Blood Deficiency, Kidney Essence Deficiency, Yin Deficiency, or Phlegm-Damp accumulation. In modern biomedical language, these may be interpreted as conceptual parallels to impaired microcirculation, reduced metabolic reserve, poor tissue nourishment, degenerative aging biology, chronic dryness or oxidative stress, and fluid dysregulation. These are not exact equivalents. They are clinical frameworks used to guide individualized care.

Translating Ayurvedic Concepts into Biomedical Language

Ayurvedic concepts such as Vata, Pitta, Kapha, Rakta Dhatu, Majja Dhatu, and Ojas may be interpreted through the lens of nervous system regulation, inflammatory balance, circulation, tissue nourishment, neural integrity, and resilience. For macular hole, an Ayurvedic-informed NRT plan may emphasize stabilizing degenerative stress, supporting retinal nourishment, regulating inflammatory heat, and strengthening systemic vitality. These are interpretive frameworks, not direct biomedical definitions.

Understanding Herbal Medicine as Network Pharmacology

Modern research increasingly studies herbal medicine through network pharmacology, systems biology, transcriptomics, proteomics, and metabolomics. A single herb can contain many bioactive compounds. A formula can contain hundreds or thousands of phytochemicals that may influence oxidative stress, inflammation, mitochondrial function, vascular regulation, immune signaling, and cellular resilience. This does not prove that any herb closes a macular hole. It supports the idea that botanical medicine can be investigated as a multi-target biological approach rather than a single-compound intervention.

Frequently Asked Questions on Macular Hole

Selected References for Scientific Support

• Duker JS, Kaiser PK, Binder S, et al. The International Vitreomacular Traction Study Group classification of vitreomacular adhesion, traction, and macular hole. Ophthalmology. 2013;120(12):2611-2619. This landmark classification defined full-thickness macular hole by OCT and categorized holes by size, cause, and vitreomacular traction status.
• Steel DHW, Lotery AJ. Idiopathic vitreomacular traction and macular hole: a comprehensive review of pathophysiology, diagnosis, and treatment. Eye. 2013;27(Suppl 1):S1-S21. This review summarizes the vitreomacular traction sequence, diagnostic concepts, and macular hole pathophysiology.
• Bikbova G, Oshitari T, Baba T, Yamamoto S, Mori K. Pathogenesis and Management of Macular Hole. Journal of Ophthalmology. 2019;2019:3467381. This review discusses macular hole as a vitreomacular interface disorder and summarizes evolving pathogenesis concepts.
• Majumdar S, Tripathy K. Macular Hole. StatPearls. Updated 2023. This clinical reference describes macular hole as a partial- or full-thickness neurosensory retinal defect at the center of the macula and reviews etiology, staging, symptoms, OCT evaluation, and prognosis.
• Bringmann A, Wiedemann P. Müller glial cells in retinal disease. Ophthalmologica. 2012;227(1):1-19. This work and related Müller cell literature describe the central role of Müller cells in retinal support, fluid regulation, neurotransmitter clearance, and tissue homeostasis.
• Bringmann A, Syrbe S, Gorner K, et al. The primate fovea: Structure, function and development. Progress in Retinal and Eye Research. 2018;66:49-84. This review explains foveal architecture and the role of glial and neuronal specialization in central vision.
• Bringmann A, Unterlauft JD, Barth T, Wiedemann R, Rehak M, Wiedemann P. Spontaneous closure of small full-thickness macular holes: presumed role of Müller cells. Acta Ophthalmologica. 2020;98(4):e447-e456. This study discusses spontaneous closure of small full-thickness macular holes and possible Müller-cell bridging mechanisms.
• Saxena S, et al. Pathoanatomical aspects of macular hole closure. Indian Journal of Ophthalmology. 2024. This paper discusses OCT-based pathoanatomical concepts in macular hole closure, including glial bridging and outer retinal restoration.
• Bodhankar PU, et al. Postoperative microstructural remodeling and functional outcome after idiopathic full-thickness macular hole repair. Indian Journal of Ophthalmology. 2022. This study evaluates OCT microstructural changes including external limiting membrane and ellipsoid zone integrity.
• Yang J, et al. Ellipsoid Zone and External Limiting Membrane-Related Parameters on Spectral-Domain Optical Coherence Tomography and Visual Outcome after Macular Hole Surgery. Frontiers in Medicine. 2021;8:779602. This study supports the importance of ellipsoid zone integrity, thickness, and reflectivity as visual outcome biomarkers.
• Kimura A, Namekata K, Guo X, Noro T, Harada C, Harada T. Neuroprotection, growth factors and BDNF-TrkB signalling in retinal degeneration. International Journal of Molecular Sciences. 2016;17(9):1584. This review summarizes neurotrophic and neuroprotective mechanisms in retinal disease.
• Kugler EC, Greenwood J, MacDonald RB. The neuro-glial-vascular unit: The role of glia in neurovascular unit formation and dysfunction. Frontiers in Cell and Developmental Biology. 2021;9:732820. This review supports the concept that retinal function depends on integrated neuronal, glial, and vascular interactions.
• Bringmann A, Pannicke T, Grosche J, et al. Müller cells in the healthy and diseased retina. Progress in Retinal and Eye Research. 2006;25(4):397-424. This classic review describes Müller cells as central regulators of retinal extracellular homeostasis, ions, water, pH, and neurotransmitters.
• Catalani E, et al. Targeting mitochondrial dysfunction and oxidative stress to prevent retinal degeneration. International Journal of Molecular Sciences. 2023. This review discusses mitochondrial dysfunction and oxidative stress as general retinal disease mechanisms.
• Lin D, De La Pena I, Lin L, et al. The neuroprotective role of acupuncture and activation of the BDNF signaling pathway. Evidence-Based Complementary and Alternative Medicine. 2014;2014:870596. This review discusses preclinical evidence that acupuncture may influence neuroprotective pathways including BDNF signaling; direct macular hole-specific clinical evidence remains limited.