• 3D bioprinting
• Cell therapy
• Glaucoma
• Neuroprotection
• Regenerative medicine
• Retinal diseases
• Retinal ganglion cells
• Retinal organoids
• Retinal regeneration
• Stem cell therapy
• Trabecular meshwork

• Exosome
• extracellular vesicles
• glaucoma
• miRNA

• Anti-inflammatory response
• Bone marrow-mesenchymal stromal cells (BM-MSCs)
• Hematopoietic support
• MSC reprogramming
• Transcriptomic analysis

• Humans
• Mesenchymal Stem Cells/metabolism
• Early Growth Response Protein 1/genetics
• Early Growth Response Protein 1/metabolism
• Transcriptome
• Gene Expression Profiling
• Cells, Cultured
• Hematopoietic Stem Cells/metabolism
• Bone Marrow Cells/metabolism

• glaucoma
• neuroprotection
• retinal neurodegeneration

• excitotoxicity
• glaucoma therapeutic approaches
• neurodegeneration
• neuroinflammation
• neuroprotection
• oxidative stress

• Cornea
• optometry
• regenerative medicine
• retina
• stem cell

• Humans
• Australia
• Female
• Male
• Optometrists
• Middle Aged
• Adult
• Health Knowledge, Attitudes, Practice
• Stem Cell Transplantation
• Surveys and Questionnaires
• Optometry
• Eye Diseases/therapy
• Aged

• Biomarkers
• exosomes
• micro-vesicles

• Exosomes/metabolism
• Humans
• Animals
• Biomarkers/metabolism

• Animals
• Humans
• Neuroprotection
• Nanomedicine
• Glaucoma/drug therapy
• Intraocular Pressure
• Stem Cells
• Disease Models, Animal

• glaucoma
• mesenchymal stromal cell
• ocular hypertension
• optic nerve head
• optical coherence tomography
• rabbit

• Type II diabetes mellitus
• acute respiratory distress syndrome
• human umbilical cord-derived mesenchymal stem cells
• lipopolysaccharide
• non-communicable disease

• Humans
• Diabetes Mellitus, Type 2/complications
• Diabetes Mellitus, Type 2/therapy
• Respiratory Distress Syndrome/therapy
• Inflammation
• COVID-19/therapy
• Mesenchymal Stem Cells
• Mesenchymal Stem Cell Transplantation
• Umbilical Cord

• FRGS/1/2020/SKK06/UPM/02/16 Ministry of Higher Education of Malaysia

• Apoptosis
• Glaucoma
• Necroptosis
• Pyroptosis
• Retinal ganglion cells

• Animals
• Retinal Ganglion Cells/metabolism
• Intraocular Pressure
• Glaucoma/therapy
• Glaucoma/metabolism
• Regulated Cell Death
• Neuroprotection
• Disease Models, Animal

• S20210026020013 College Students' Innovation and Entrepreneurship Project
• KLET-202210 Key Laboratory of Emergency and Trauma of Ministry of Education (Hainan Medical University)
• 81971891 National Natural Science Foundation of China
• College Students’ Innovation and Entrepreneurship Project

• CM
• MSC
• conditioned medium
• exosome
• eye
• mesenchymal stem cell
• ocular disease
• regenerative medicine
• secretome

• Culture Media, Conditioned/pharmacology
• Secretome
• Mesenchymal Stem Cells

• CNS
• axonal regeneration
• brain
• electrical stimulation
• electroacupuncture
• electromagnetic stimulation
• optic nerve
• red light therapy
• retina
• ultrasound therapy

• Animals
• Humans
• Axons/metabolism
• Neuroprotection
• Rejuvenation
• Nerve Regeneration/physiology
• Retinal Ganglion Cells/metabolism
• Mammals

• COVID-19
• Lung disease
• Mesenchymal stem cells

• EMT
• Human Wharton’s jelly mesenchymal stem cell secretome
• Neuroprotection
• PVR
• RPE

• Shiraz University of Medical Sciences Shiraz University of Medical Sciences

• amniotic fluid stem cells
• sorting
• stemness
• transcriptome

• bronchiectasis
• congenital abnormalities
• interstitial lung disease
• primary ciliary dyskinesia

• glaucomatous optic neuropathy
• glutamate
• optic nerve protection

• RGC
• exosome
• mesenchymal stem cell-derived secretome
• neuroprotection
• neuroregeneration
• optic neuropathy

• brain-derived neurotrophic factor
• glaucoma
• neurodegeneration
• neuroprotection
• retina
• retinal ganglion cell

• Ministry of Higher Education, Malaysia

The purpose of this study was to explore the therapeutic effect of human umbilical cord mesenchymal stem cell (HUMSC) transplantation alone or assisted with ultrasound targeted microbubble destruction (UTMD) on optic neuropathy in a novel and practical model of experimental glaucoma in rabbits.

Eight New Zealand white healthy rabbits were used as the control group (group A). Twenty-four experimental glaucomatous rabbits were established as described previously and randomly divided into three groups: (1) received no treatment (group B); (2) received intravitreal transplantation of HUMSCs (group C); and (3) received UTMD-assisted intravitreal transplantation of HUMSCs (group D). After 4 weeks of treatment, the distribution of HUMSCs, retinal thickness, layer structure, retinal ganglion cells (RGCs), and their axons were examined.

After 4 weeks of treatment, HUMSCs were successfully scattered under the retina. HUMSC transplantation significantly increased the regeneration of RGCs and their axons, and restored the retinal structure in glaucomatous rabbits. Moreover, the application of UTMD enhances HUMSC distribution and achieved more significant therapeutic effect.

Intravitreal transplantation of HUMSCs effectively repaired glaucomatous optic nerve injury, and UTMD enhanced the successful delivery of HUMSCs into injured retina, promoting its therapeutic effects remarkably.

This study demonstrated that HUMSC transplantation repaired the glaucoma-caused nerve injury significantly and the combination of UTMD can augment the therapeutic effect further, which has important clinical guiding significance for the development of therapeutic strategies of glaucoma.

• Mesenchymal stem cells
• extracellular vesicles
• ophthalmic diseases
• therapy

Therapeutic agents that are able to prevent or attenuate inflammation and ischemia-induced injury of neural and retinal cells could be used for the treatment of neural and retinal diseases. Exosomes derived from adipose tissue-sourced mesenchymal stem cells (AT-MSC-Exos) are extracellular vesicles that contain neurotrophins, immunoregulatory and angio-modulatory factors secreted by their parental cells. AT-MSC-Exos are enriched with bioactive molecules (microRNAs (miRNAs), enzymes, cytokines, chemokines, immunoregulatory, trophic, and growth factors), that alleviate inflammation and promote the survival of injured cells in neural and retinal tissues. Due to the nano-sized dimension and bilayer lipid envelope, AT-MSC-Exos easily bypass blood–brain and blood–retinal barriers and deliver their cargo directly into the target cells. Accordingly, a large number of experimental studies demonstrated the beneficial effects of AT-MSC-Exos in the treatment of neural and retinal diseases. By delivering neurotrophins, AT-MSC-Exos prevent apoptosis of injured neurons and retinal cells and promote neuritogenesis. AT-MSC-Exos alleviate inflammation in the injured brain, spinal cord, and retinas by delivering immunoregulatory factors in immune cells, suppressing their inflammatory properties. AT-MSC-Exos may act as biological mediators that deliver pro-angiogenic miRNAs in endothelial cells, enabling re-vascularization of ischemic neural and retinal tissues. Herewith, we summarized current knowledge about molecular mechanisms which were responsible for the beneficial effects of AT-MSC-Exos in the treatment of neural and retinal diseases, emphasizing their therapeutic potential in neurology and ophthalmology.

• adipose tissue-derived mesenchymal stem cells
• exosomes
• neural diseases
• retinal diseases
• therapy

• exosomes
• mesenchymal stem cells
• ncRNAs
• ocular diseases
• regenerative medicine

• Exosomes
• Mesenchymal stromal cells
• Optic nerve injury
• Optic nerve regeneration

• Exosomes/metabolism
• Humans
• Nerve Regeneration/physiology
• Optic Nerve/metabolism
• Optic Nerve Injuries/metabolism

• Cellular therapy
• Glaucoma
• Immunomodulation
• Mesenchymal stem cell
• Microglia
• Neuroprotection
• Retinal ganglion cell

• Anti-myelin oligodendrocyte glycoprotein associated disease
• Autoimmune disorder
• Exosome
• Extracellular vesicles
• MicroRNA
• Multiple Sclerosis
• Neurodegeneration
• Neuromyelitis optica spectrum disorder
• Optic nerve
• Optic neuritis
• Retina
• Retinal ganglion cells
• Stem cells

• Animals
• Extracellular Vesicles
• Mesenchymal Stem Cells
• Myelin-Oligodendrocyte Glycoprotein
• Neuromyelitis Optica/complications
• Optic Neuritis/complications
• Optic Neuritis/therapy

• DE027404 NIDCR NIH HHS
• P30 EY001792 NEI NIH HHS
• R01 DE027404 NIDCR NIH HHS
• P30 EY026877 NEI NIH HHS
• EY001792 NEI NIH HHS
• UL1 TR002003 NCATS NIH HHS
• EY028690 NEI NIH HHS
• I01 BX002625 BLRD VA
• R21 EY028690 NEI NIH HHS
• National Eye Institute
• National Institute of Dental and Craniofacial Research
• Office of Academic Affiliations, Department of Veterans Affairs
• National Center for Research Resources
• National Multiple Sclerosis Society
• BrightFocus Foundation
• Glaucoma Research Foundation

Traditional Chinese medicine (TCM) has a long history of treating glaucoma with remarkable effects, but there is no clear conclusion on its mechanism.

Network pharmacology and molecular docking were used to analyze the mechanism and targets of TCM in the treatment of glaucoma, and baicalein was used to treat chronic ocular hypertension animal models rats for observation.

The results of animal experiments showed that baicalein could significantly reduce intraocular pressure (IOP) in a rat model of chronic ocular hypertension and protect the structure of the retina and optic nerve, as shown by hematoxylin–eosin (H&E) staining and transmission electron microscopy (TEM). Reducing the apoptosis of retinal ganglion cells (RGCs) by upregulating the expression of the antiapoptotic protein BCL-2 is basically consistent with the results of molecular docking. In the network pharmacology analysis, many key proteins of biological pathways involved in the herbal therapeutic processes in glaucoma, such as threonine kinase 1 (AKT1, core protein of PI3K/AKT signaling), tumor protein p53 (TP53, a tumor suppressor gene coding tumor protein P53), signal transducer and activator of transcription 3 (STAT3, core protein of JAK/STAT signaling), interleukin 6 (IL-6) and interleukin 17 (IL-17, proinflammatory factors), were identified. Their interactions built complicated chain reactions in the process of glaucoma.

By combining the analysis of network pharmacology and animal experimental results, baicalein could effectively improve the symptoms of glaucoma and reduce RGC apoptosis, suggesting that the potential mechanism of TCM in treating glaucoma is related to regulating inflammation and cellular immunity and reducing apoptosis.

• Baicalein
• Experimental validation
• Glaucoma
• Network pharmacological

Damage to the optic nerve and the death of associated retinal ganglion cells (RGCs) by elevated intraocular pressure (IOP), also known as glaucoma, is responsible for visual impairment and blindness in millions of people worldwide. The ocular hypertension (OHT) and the deleterious mechanical forces it exerts at the back of the eye, at the level of the optic nerve head/optic disc and lamina cribosa, is the only modifiable risk factor associated with glaucoma that can be treated. The elevated IOP occurs due to the inability of accumulated aqueous humor (AQH) to egress from the anterior chamber of the eye due to occlusion of the major outflow pathway, the trabecular meshwork (TM) and Schlemm’s canal (SC). Several different classes of pharmaceutical agents, surgical techniques and implantable devices have been developed to lower and control IOP. First-line drugs to promote AQH outflow via the uveoscleral outflow pathway include FP-receptor prostaglandin (PG) agonists (e.g., latanoprost, travoprost and tafluprost) and a novel non-PG EP2-receptor agonist (omidenepag isopropyl, Eybelis^®). TM/SC outflow enhancing drugs are also effective ocular hypotensive agents (e.g., rho kinase inhibitors like ripasudil and netarsudil; and latanoprostene bunod, a conjugate of a nitric oxide donor and latanoprost). One of the most effective anterior chamber AQH microshunt devices is the Preserflo^® microshunt which can lower IOP down to 10–13 mmHg. Other IOP-lowering drugs and devices on the horizon will be also discussed. Additionally, since elevated IOP is only one of many risk factors for development of glaucomatous optic neuropathy, a treatise of the role of inflammatory neurodegeneration of the optic nerve and retinal ganglion cells and appropriate neuroprotective strategies to mitigate this disease will also be reviewed and discussed.

• aqueous humor
• drug discovery
• glaucoma
• intraocular pressur
• neurodegenaration
• neuroprotection
• pharmacology

• Diabetic retinopathy
• Eye diseases
• Glaucoma
• Mesenchymal stem cells
• Regenerative medicine
• Retinitis pigmentosa

• Caenorhabditis elegans
• Parkinson's disease
• alpha-synuclein
• mesenchymal stem cells
• secretome

Overall, the human organism requires the production of ∼1 trillion new blood cells per day. Such goal is achieved via hematopoiesis occurring within the bone marrow (BM) under the tight regulation of hematopoietic stem and progenitor cell (HSPC) homeostasis made by the BM microenvironment. The BM niche is defined by the close interactions of HSPCs and non-hematopoietic cells of different origin, which control the maintenance of HSPCs and orchestrate hematopoiesis in response to the body’s requirements. The activity of the BM niche is regulated by specific signaling pathways in physiological conditions and in case of stress, including the one induced by the HSPC transplantation (HSCT) procedures. HSCT is the curative option for several hematological and non-hematological diseases, despite being associated with early and late complications, mainly due to a low level of HSPC engraftment, impaired hematopoietic recovery, immune-mediated graft rejection, and graft-versus-host disease (GvHD) in case of allogenic transplant. Mesenchymal stromal cells (MSCs) are key elements of the BM niche, regulating HSPC homeostasis by direct contact and secreting several paracrine factors. In this review, we will explore the several mechanisms through which MSCs impact on the supportive activity of the BM niche and regulate HSPC homeostasis. We will further discuss how the growing understanding of such mechanisms have impacted, under a clinical point of view, on the transplantation field. In more recent years, these results have instructed the design of clinical trials to ameliorate the outcome of HSCT, especially in the allogenic setting, and when low doses of HSPCs were available for transplantation.

• bone marrow niche
• hematopoietic (stem) cell transplantation
• hematopoietic stem and progenitor cell
• immunoregulation
• mesenchymal stromal cells

• mesenchymal stem cells
• optogenetic stimulation
• retinal degenerative disorders
• retinal differentiation
• retinal pigment epithelial cells

Around 40% of the population will suffer at some point in their life a disease involving tissue loss or an inflammatory or autoimmune process that cannot be satisfactorily controlled with current therapies. An alternative for these processes is represented by stem cells and, especially, mesenchymal stem cells (MSC). Numerous preclinical studies have shown MSC to have therapeutic effects in different clinical conditions, probably due to their mesodermal origin. Thereby, MSC appear to play a central role in the control of a galaxy of intercellular signals of anti-inflammatory, regenerative, angiogenic, anti-fibrotic, anti-oxidative stress effects of anti-apoptotic, anti-tumor, or anti-microbial type. This concept forces us to return to the origin of natural physiological processes as a starting point to understand the evolution of MSC therapy in the field of regenerative medicine. These biological effects, demonstrated in countless preclinical studies, justify their first clinical applications, and draw a horizon of new therapeutic strategies. However, several limitations of MSC as cell therapy are recognized, such as safety issues, handling difficulties for therapeutic purposes, and high economic cost. For these reasons, there is an ongoing tendency to consider the use of MSC-derived secretome products as a therapeutic tool, since they reproduce the effects of their parent cells. However, it will be necessary to resolve key aspects, such as the choice of the ideal type of MSC according to their origin for each therapeutic indication and the implementation of new standardized production strategies. Therefore, stem cell science based on an intelligently designed production of MSC and or their derivative products will be able to advance towards an innovative and more personalized medical biotechnology.

• MSC in vitro production
• MSC large-scale expansion
• bioreactor
• ex vivo MSC modifications
• exosomes
• extracellular vesicles
• secretome

• Animals
• Exosomes/metabolism
• Exosomes/transplantation
• Humans
• Mesenchymal Stem Cell Transplantation/methods
• Mesenchymal Stem Cell Transplantation/trends
• Mesenchymal Stem Cells/metabolism
• Regenerative Medicine/methods
• Regenerative Medicine/trends

Cell replacement therapy using mesenchymal (MSC) and other stem cells has been evaluated for diabetic retinopathy and glaucoma. This approach has significant limitations, including few cells integrated, aberrant growth, and surgical complications. Mesenchymal Stem Cell Exosomes/Extracellular Vesicles (MSC EVs), which include exosomes and microvesicles, are an emerging alternative, promoting immunomodulation, repair, and regeneration by mediating MSC’s paracrine effects. For the clinical translation of EV therapy, it is important to determine the cellular destination and time course of EV uptake in the retina following administration. Here, we tested the cellular fate of EVs using in vivo rat retinas, ex vivo retinal explant, and primary retinal cells. Intravitreally administered fluorescent EVs were rapidly cleared from the vitreous. Retinal ganglion cells (RGCs) had maximal EV fluorescence at 14 days post administration, and microglia at 7 days. Both in vivo and in the explant model, most EVs were no deeper than the inner nuclear layer. Retinal astrocytes, microglia, and mixed neurons in vitro endocytosed EVs in a dose-dependent manner. Thus, our results indicate that intravitreal EVs are suited for the treatment of retinal diseases affecting the inner retina. Modification of the EV surface should be considered for maintaining EVs in the vitreous for prolonged delivery.

• astrocytes
• exosomes
• extracellular vesicles
• in vivo imaging
• ischemia
• microglia
• retina
• retinal ganglion cells

• Rho kinase inhibitors
• brimonidine
• citicoline
• growth factors
• retinal ganglion cells (RGCs)
• stem cell therapy

• Akt
• Erk
• excitotoxicity
• neuroprotection
• peptide

The enormous advances in stem cell research have generated high expectations in the development of new therapies to repair or regenerate damaged tissues. For this reason, laboratory studies of stem cells enable scientists to learn about cells’ essential properties. Specifically, in recent years, therapies based on mesenchymal stem cells have become an interesting alternative for the treatment of different complex pathologies in veterinary medicine. Mesenchymal stem cells secrete a wide variety of therapeutic elements such as bioactive molecules and extracellular vesicles (e.g., exosomes). Thus, it is essential to characterize them before future use as biotechnological products. Therefore, the objective of this study was to determine and compare their protein profile to understand better the mechanisms of action of these components and facilitate their possible use in future therapies. The data demonstrate the existence of different proteins responsible for the biological effects of cells. In addition, these approaches and techniques can contribute to the better prediction of clinical outcomes of mesenchymal stem cell treatment.

Mesenchymal stem cells (MSCs) have been shown to have therapeutic efficacy in different complex pathologies in feline species. This effect is attributed to the secretion of a wide variety of bioactive molecules and extracellular vesicles, such as exosomes, with significant paracrine activity, encompassed under the concept of the secretome. However, at present, the exosomes from feline MSCs have not yet been studied in detail. The objective of this study is to analyze and compare the protein profiles of the secretome as a whole and its exosomal fraction from feline adipose-derived MSCs (fAd-MSCs). For this, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and Protein–Protein Interaction Networks Functional Enrichment Analysis (STRING) were utilized. A total of 239 proteins were identified in the secretome, and 228 proteins specific to exosomes were identified, with a total of 133 common proteins. The proteins identified in the secretome were located in the extracellular regions and in the cytoplasm, while the exosomal proteins were located mainly in the membrane, cytoplasm and cytosol. Regarding function, in the secretome, proteins involved in different metabolic pathways, in pathways related to the immune system and the endocrine system and in the processing of proteins in the endoplasmic reticulum predominated. In contrast, proteins specific to exosomes were predominantly associated with endocytosis, cell junctions, platelet activation and other cell signaling pathways. The possible future use of the secretome, or some of its components, such as exosomes, would provide a non-cell-based therapeutic strategy for the treatment of different diseases that would avoid the drawbacks of cell therapy.

• exosomes
• feline
• mesenchymal stem cells
• secretome
• ultrahigh-performance liquid chromatography-high-resolution mass spectrometry (UHPLC–HRMS)

Retinal degenerative diseases (RDDs) are a group of diseases contributing to irreversible vision loss with yet limited therapies. Stem cell-based therapy is a promising novel therapeutic approach in RDD treatment. Mesenchymal stromal/stem cells (MSCs) have emerged as a leading cell source due to their neurotrophic and immunomodulatory capabilities, limited ethical concerns, and low risk of tumor formation. Several pre-clinical studies have shown that MSCs have the potential to delay retinal degeneration, and recent clinical trials have demonstrated promising safety profiles for the application of MSCs in retinal disease. However, some of the clinical-stage MSC therapies have been unable to meet primary efficacy end points, and severe side effects were reported in some retinal “stem cell” clinics. In this review, we provide an update of the interaction between MSCs and the RDD microenvironment and discuss how to balance the therapeutic potential and safety concerns of MSCs' ocular application.

• immunomodulation
• inflammation
• interaction
• licensing
• mesenchymal stem cells
• retinal degenerative diseases
• trophic
• tunneling nanotubes

Ischemic retinopathies (IRs), such as retinopathy of prematurity and diabetic retinopathy, are characterized by an initial phase of microvascular degeneration that results in retinal ischemia, followed by exaggerated pathologic neovascularization (NV). Mesenchymal stromal cells (MSCs) have potent pro-angiogenic and anti-inflammatory properties associated with tissue repair and regeneration, and in this regard exert protection to neurons in ischemic and degenerative conditions; however, the exact mechanisms underlying these functions remain largely unknown. Class III Semaphorins (A–G) are particularly implicated in regulating neural blood supply (as well as neurogenesis) by suppressing angiogenesis and affecting myeloid cell function; this is the case for distinct neuropillin-activating Sema3A as well as PlexinD1-activating Sema3E; but during IR the former Sema3A increases while Sema3E decreases. We investigated whether retinal vascular repair actions of MSCs are exerted by normalizing Semaphorin and downstream cytokines in IR. Intravitreal administration of MSCs or their secretome (MSCs-conditioned media [MSCs-CM]) significantly curtailed vasoobliteration as well as aberrant preretinal NV in a model of oxygen-induced retinopathy (OIR). The vascular repair effects of MSCs-CM in the ischemic retina were associated with restored levels of Sema3E. Vascular benefits of MSCs-CM were reversed by anti-Sema3E; while intravitreal injection of anti-angiogenic recombinant Sema3E (rSema3E) in OIR-subjected mice reproduced effects of MSCs-CM by inhibiting as expected preretinal NV but also by decreasing vasoobliteration. To explain these opposing vascular effects of Sema3E we found in OIR high retinal levels, respectively, of the pro- and anti-angiogenic IL-17A and Sema3A-regulating IL-1β; IL-17A positively affected expression of IL-1β. rSema3E decreased concentrations of these myeloid cell-derived pro-inflammatory cytokines in vitro and in vivo. Importantly, IL-17A suppression by MSCs-CM was abrogated by anti-Sema3E neutralizing antibody. Collectively, our findings provide novel evidence by which MSCs inhibit aberrant NV and diminish vasoobliteration (promoting revascularization) in retinopathy by restoring (at least in part) neuronal Sema3E levels that reduce pathological levels of IL-17A (and in turn other proinflammatory factors) in myeloid cells. The ability of MSCs to generate a microenvironment permissive for vascular regeneration by controlling the production of neuronal factors involved in immunomodulatory activities is a promising opportunity for stem cell therapy in ocular degenerative diseases.

• interleukin-17A
• ischemic retinopathies
• mesenchymal stem cells
• semaphorin 3E
• vascular regeneration

• ERG
• Electroretinogram
• Glaucoma
• Mesenchymal stem cells

• drug delivery
• exosomes
• extracellular vesicles
• ocular diseases
• retina

• biomaterial
• ecto-mesenchymal
• electrophysiology
• myelin
• neglected wound
• nerve repair
• neurofilament
• stem cells
• syngenic transplantation

• Animals
• Axons/metabolism
• Disease Models, Animal
• Locomotion
• Mesenchymal Stem Cell Transplantation
• Muscle, Skeletal/metabolism
• Muscle, Skeletal/pathology
• Myelin Sheath/metabolism
• Nerve Regeneration
• Olfactory Mucosa/cytology
• Olfactory Mucosa/transplantation
• Organ Size
• Peripheral Nerve Injuries/etiology
• Peripheral Nerve Injuries/metabolism
• Peripheral Nerve Injuries/pathology
• Peripheral Nerve Injuries/therapy
• Peroneal Nerve/injuries
• Peroneal Nerve/metabolism
• Peroneal Nerve/physiopathology
• Rats

• PE-TOU-15 Fondation de l'Avenir pour la Recherche Médicale Appliquée
• Recurrent funding Centre National de la Recherche Scientifique
• recurrent funding Aix-Marseille Université

Glaucoma is one of the leading causes of irreversible blindness in the world and remains a major public health problem. To date, incomplete knowledge of this disease’s pathophysiology has resulted in current therapies (pharmaceutical or surgical) unfortunately having only a slowing effect on disease progression. Recent research suggests that glaucomatous optic neuropathy is a disease that shares common neuroinflammatory mechanisms with “classical” neurodegenerative pathologies. In addition to the death of retinal ganglion cells (RGCs), neuroinflammation appears to be a key element in the progression and spread of this disease. Indeed, early reactivity of glial cells has been observed in the retina, but also in the central visual pathways of glaucoma patients and in preclinical models of ocular hypertension. Moreover, neuronal lesions are not limited to retinal structure, but also occur in central visual pathways. This review summarizes and puts into perspective the experimental and clinical data obtained to date to highlight the need to develop neuroprotective and immunomodulatory therapies to prevent blindness in glaucoma patients.

• central visual pathway
• neuroinflammation
• neuronal degeneration
• ocular hypertension