Changes in BDNF and MAPK Signaling Pathways in Experimental Glaucoma

Fabiani, Carlotta; Cerri, Elisa

doi:10.4172/2155-9570.1000530

Cited by 5 publications

(3 citation statements)

References 33 publications

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“…The functional activity of BDNF is manifested through its interaction with the TrkB receptor, leading to the activation of intracellular signaling pathways associated with cell viability, including the phosphatidylinositol-3 kinase (PI-3 K)/Akt and extracellular signal-regulated kinases 1/2 (Erk1/2) pathways. Both of these signaling pathways have been implicated in experimental glaucoma ( Cheng et al, 2002 ; Carlotta et al, 2016 ; Liang et al, 2019 ). There are several studies using different models of glaucoma that indicate that local administration of BDNF to the eye results in reduced loss of RGCs.…”

Section: Molecular Mechanisms Of Glaucoma Developmentmentioning

confidence: 99%

Molecular pathways in experimental glaucoma models

Bugara,

Pacwa,

Smedowski

2024

Front. Neurosci.

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Glaucoma is a complex and progressive disease that primarily affects the optic nerve axons, leading to irreversible vision loss. Although the exact molecular mechanisms underlying glaucoma pathogenesis are not fully understood, it is believed that except increased intraocular pressure, a combination of genetic and environmental factors play a role in the development of the disease. Animal models have been widely used in the study of glaucoma, allowing researchers to better understand the underlying mechanisms of the disease and test potential treatments. Several molecular pathways have been implicated in the pathogenesis of glaucoma, including oxidative stress, inflammation, and excitotoxic-induced neurodegeneration. This review summarizes the most important knowledge about molecular mechanisms involved in the glaucoma development. Although much research has been done to better understand the molecular mechanisms underlying this disease, there is still much to be learned to develop effective treatments and prevent vision loss in those affected by glaucoma.

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Section: Molecular Mechanisms Of Glaucoma Developmentmentioning

confidence: 99%

Molecular pathways in experimental glaucoma models

Bugara,

Pacwa,

Smedowski

2024

Front. Neurosci.

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“…TrkB is also highly expressed in the RGC dendrites and cell bodies [79]. Although the primary source of BDNF supply for RGCs is known to be the brain, studies have also demonstrated that there is a level of local expression of this neurotrophin in the RGCs, Müller glial cells, and astrocytes [80]. Following BDNF binding, TrkB is activated through dimerization and autophosphorylation on its critical intracellular tyrosine residues [61].…”

Section: Bdnf/trkb Signalingmentioning

confidence: 99%

Molecular Mechanisms of Glaucoma Pathogenesis with Implications to Caveolin Adaptor Protein and Caveolin-Shp2 Axis

Abbasi,

Gupta,

Chitranshi

et al. 2024

Aging and disease

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Glaucoma is a common retinal disorder characterized by progressive optic nerve damage, resulting in visual impairment and potential blindness. Elevated intraocular pressure (IOP) is a major risk factor, but some patients still experience disease progression despite IOP-lowering treatments. Genome-wide association studies have linked variations in the Caveolin1/2 (CAV-1/2) gene loci to glaucoma risk. Cav-1, a key protein in caveolae membrane invaginations, is involved in signaling pathways and its absence impairs retinal function. Recent research suggests that Cav-1 is implicated in modulating the BDNF/TrkB signaling pathway in retinal ganglion cells, which plays a critical role in retinal ganglion cell (RGC) health and protection against apoptosis. Understanding the interplay between these proteins could shed light on glaucoma pathogenesis and provide potential therapeutic targets.

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“…Several models of glaucoma have indicated that inflammatory components can directly link elevated IOP with retinal degeneration . As a result, the expression of inflammatory molecules, including nitric oxide, interleukins (ILs), p38 MAPK, and prostaglandin E2 (PGE2), are increased in progressive glaucoma. Furthermore, inflammatory progression is also associated with the increased expression of matrix metalloproteinases (MMPs), which consequently induce the degradations of extracellular matrix (ECM) components such as stromal collagen and retinal laminin .…”

Section: Introductionmentioning

confidence: 99%

Dendritic Effects of Injectable Biodegradable Thermogels on Pharmacotherapy of Inflammatory Glaucoma‐Associated Degradation of Extracellular Matrix

Nguyen

Luo

Lai

2019

Adv Healthcare Materials

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111.8 million people worldwide by 2040. [1] High intraocular pressure (IOP) has been considered the major indicator for diagnosing glaucoma, and the reduction of elevated IOP is the current clinical approach used to prevent disease progression. [2] Several models of glaucoma have indicated that inflammatory components can directly link elevated IOP with retinal degeneration. [3][4][5][6] As a result, the expression of inflammatory molecules, including nitric oxide, [7] interleukins (ILs), [8] p38 MAPK, [9] and prostaglandin E2 (PGE2), [10] are increased in progressive glaucoma. Furthermore, inflammatory progression is also associated with the increased expression of matrix metalloproteinases (MMPs), [11] which consequently induce the degradations of extracellular matrix (ECM) components such as stromal collagen [12] and retinal laminin. [13] It is noteworthy that ECM possesses adhesive characteristics that can regulate cell function and survival; changes in composition and status of ECM components can result in disruptions of cell-cell and cell-ECM interactions, consequently inducing cell apoptosis. [14][15][16] Therefore, it is highly imperative to develop new therapies for effectively attenuating the upregulation of inflammatory molecules as well as the degradation of stromal collagen and retinal laminin in glaucoma.Dendrimers, which are synthetic macromolecules with well-defined 3D shapes that contain a central core, repeating branched units, and dense shells with terminal functional groups, have been emerging in polymeric architecture in biomedical engineering. These macromolecules can increase the water solubility, bioavailability, and biocompatibility of pharmaceutical agents and show promise for practical use as drug carriers. [17] More interestingly, dendrimers can also be exploited as a key component that regulates the encapsulation and release of other carriers to achieve improved drug delivery. For example, the interior cavities of polyamidoamine (PAMAM) dendrimers can entrap drug molecules, while their amine-terminated surface groups are available for crosslinking with poly(ethylene glycol) mono/diacrylate to generate hydrogel materials with the ability to release drugs in a sustained manner through a twostage process, which involves the release of drug-entrapping dendrimers from degradable hydrogels and the release of drug The development of advanced drug delivery systems with extensively sustained release and multiple functions is highly imperative for effective attenuation of the degradation of ocular extracellular matrix that is associated with inflammatory glaucoma. Here, the generation of amine-terminated polyamidoamine dendrimers in an injectable biodegradable thermogel is demonstrated to be important for achieving prolonged drug release profiles and potent anti-inflammatory effects. Among various generations (Gx, x = 0, 1, 3, 5), third-generation G3 is proved as the most effective material for optimizing the synergistic effects of gelatin and poly(N-isopropylacrylamide) and generating a thermo...

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Changes in BDNF and MAPK Signaling Pathways in Experimental Glaucoma

Cited by 5 publications

References 33 publications

Molecular pathways in experimental glaucoma models

Molecular pathways in experimental glaucoma models

Molecular Mechanisms of Glaucoma Pathogenesis with Implications to Caveolin Adaptor Protein and Caveolin-Shp2 Axis

Dendritic Effects of Injectable Biodegradable Thermogels on Pharmacotherapy of Inflammatory Glaucoma‐Associated Degradation of Extracellular Matrix

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