Medication Trends for Age-Related Macular Degeneration

Cho, Yeon-Kyoung; Park, Dae-Hun; Jeon, In-Chul

doi:10.3390/ijms222111837

Cited by 24 publications

(17 citation statements)

References 111 publications

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“…Evaluation of VEGF level cause blood vessels growth and leakage, which is the primary cause of wet AMD [33]. Based on this theory, anti-VEGF therapies are commonly used to treat with the wet AMD [34]. The patients must be injected with the anti-VEGF drugs into the eye for every four to twelve weeks depending on their response [34].…”

Section: Exosomal Protein Profile In Anti-vegf Treatment Amdmentioning

confidence: 99%

Proteomic Profiling of Aqueous Humor Exosomes from Age-related Macular Degeneration Patients

Tsai¹,

Chen²,

Wu³

et al. 2022

Int. J. Med. Sci.

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Purpose:The alteration of the exosomal proteins in the aqueous humor (AH) is linked to the development of eye diseases. The goal of this study was to examine the exosomal protein profile of patients with age-related macular degeneration (AMD) to better understand their role in the pathogenesis of AMD. Methods: Exosomes were isolated from the AH of 28 AMD and 25 control eyes. The quality, concentration, and size distribution of exosomes were measured using a nanoparticle tracking analysis system (NTA). Total exosomal proteins from each sample were purified and digested with trypsin for liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis. Results: Based on LC-MS/MS analysis, we got 105 exosomal peptides from AMD and control patients. Gene ontology (GO) analysis in the biology process revealed that exosomal proteins of AMD were enriched in the lipoprotein metabolic process. T-test analysis revealed six exosomal proteins in patients with AMD were significantly different from controls. Comparing the exosomal protein profile of AMD patients who were receiving anti-VEGF therapy, we observed the amount of two proteins decreased with the duration of the anti-VEGF treatment time. Conclusions: In this study, we successfully isolated and purified AH exosomes. Our results provide pioneering findings for the exosomal protein profile in AMD development and under therapy. These unique proteins could be the new targets for drug discovery or biological markers for evaluating therapeutic efficacy.

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Section: Exosomal Protein Profile In Anti-vegf Treatment Amdmentioning

confidence: 99%

Proteomic Profiling of Aqueous Humor Exosomes from Age-related Macular Degeneration Patients

Tsai¹,

Chen²,

Wu³

et al. 2022

Int. J. Med. Sci.

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“…However, despite considerable advancements in etiology, there is still no authorized medicine or effective treatment for dry AMD. Therefore, finding a successful treatment for dry AMD is more critical than it is for wet AMD [13].…”

Section: Pathophysiologymentioning

confidence: 99%

Age-Related Macular Degeneration: Epidemiology, Pathophysiology, Diagnosis, and Treatment

Vyawahare¹,

Shinde²

2022

Cureus

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The greatest global root of irremediable amaurosis in the venerable is age-related macular degeneration (AMD), a complex eye condition. Clinically, AMD is characterized as being in an early stage to late stage and initially affects the macula, which is the center of the retina (advanced AMD). Age-related cellular and metabolic imbalance are made worse by the creation of excessive amounts of free radical species, which causes mitochondrial malfunction. As a result, in AMD-affected eyes, the deprivation of melanocytes, confection, and eventually atrophy within the retinal tissue are caused by the continued proliferation of oxidative stress caused by systemic antioxidant capacity depletion.In the urbanized, industrialized world, age-related macular degeneration (AMD) is one of the major causes of central vision loss in the older age group. Although several causes and mechanisms for the dysfunction and degeneration of the retinal pigment epithelium (RPE) have previously been identified, the condition's symptoms are still not fully understood. Etiopathogenesis is still not entirely understood. As a result, the RPE fails, allowing an accumulation of aberrant misfolded proteins, due to the loss of anatomical control over oppression, altered homeostasis, dysfunctional lipid homeostasis, and failure of mitochondria.Due to the multitude of interconnected processes, numerous complicated therapy combinations will probably be the best option to deliver the best visual outcomes; these combinations will vary depending on the kind and degree of the condition being treated. Undoubtedly, this will lead to the development of customized preventative medications and, hopefully, the revelation of a potential cure. All the mechanisms involved in the etiology of AMD should be continuously probed to create covariates for other contemporaneous or future problems.

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“…In fact, cell survival and programmed cell death are intimately linked to the autophagy process and, although the specific mechanism of cell death in the RPE in AMD (py-roptosis, necroptosis, or apoptosis) is unknown, the disease could be explained by failed regulation of this cellular process [71]. Many natural products possibly constraining AMD severity have been used and investigated based on their mode of action as antiapoptosis inducers or as cell cycle arrest modulators, but the level of evidence supporting their use is low [72].…”

Section: Alterations Of Autophagosome/lysosomal and Upsmentioning

confidence: 99%

“…Management of nAMD has advanced dramatically due to the introduction of effective intravitreal treatments with anti-vascular EGF (anti-VEGF) capable of maintaining VA on a long-term basis of at least 4–5 years, although undertreatment may worsen final outcomes [131]. Unfortunately, no such advances have been made in the treatment of aAMD so far, and no effective therapy can fully prevent progression from the intermediate to the advanced stage of the disease [72, 132]. The development of atrophy in patients in whom the neovascular component is controlled also must be addressed.…”

Section: Conclusion and Consequent Therapeutic Optionsmentioning

confidence: 99%

“…In fact, some complement inhibitors are currently being tested in clinical trials to halt GA progression [135, 136], but some of these therapeutic options have shown unfavorable benefit-risk ratios and further studies are warranted [137]. Another interesting point would be that once nAMD is established, treatment with anti-VEGFs might be combined with another treatment focused on modulating subretinal inflammation as a secondary prevention of fibrosis or atrophy that can occur further along in the disease evolution and lead to additional visual loss [72, 138, 139]. Reprogramming epigenetic information may also be a future therapeutic option [130].…”

Section: Conclusion and Consequent Therapeutic Optionsmentioning

confidence: 99%

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Pathophysiology of Age-Related Macular Degeneration: Implications for Treatment

et al. 2022

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Age-related macular degeneration (AMD) is a complex, multifactorial, progressive retinal disease that affects millions of people worldwide and has become the leading cause of visual impairment in developed countries. The disease etiopathogenesis is not understood fully, although many triggers and processes that lead to dysfunction and degeneration of the retinal pigment epithelium (RPE) already have been identified. Thus, the lack of cellular control of oxidative stress, altered proteostasis, dysfunction of lipid homeostasis, and mitochondrial dysfunction form an internal feedback loop that causes the RPE to fail and allows accumulation of abnormal misfolded proteins and abnormal lipids that will form drusen. An inadequate antioxidant response, deficits in autophagy mechanisms, and dysregulation of the extracellular matrix (ECM) help to increase the deposition of abnormal drusen material over time. The drusen then act as inflammatory centers that trigger chronic inflammation of the subretinal space in which microglia and recruited macrophages also are involved, and the complement system is a key component. Choriocapillaris degeneration and nutritional influences are also classic elements recognized in the AMD pathophysiology. The genetic component of the disease is embodied in the recognition of the described risk or protective polymorphisms of some complement (mainly complement factor H, CFH) and ECM related genes (mainly age-related maculopathy susceptibility 2/high-temperature requirement protein A1, ARMS2/HTRA1). Carriers of the risk haplotype at ARMS2/HTRA1 have a higher risk of developing late AMD at a younger age. Finally, gut microbiota and epigenetics may play a role in modulating the progression to advanced AMD with the presence of local inflammatory conditions. Because of multiple implicated processes, different complex combinations of treatments will probably be the best option to obtain the best visual results; they in turn will differ depending on the type and spectrum of disease affecting individual patients or the disease stage in each patient at a specific moment. This will undoubtedly lead to personalized medicine for control and hopefully a future cure, which necessitates the continued unraveling of all the processes involved in the pathogenesis of AMD that must be understood to devise the combinations of treatments for different concurrent or subsequent problems.

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Medication Trends for Age-Related Macular Degeneration

Cited by 24 publications

References 111 publications

Proteomic Profiling of Aqueous Humor Exosomes from Age-related Macular Degeneration Patients

Proteomic Profiling of Aqueous Humor Exosomes from Age-related Macular Degeneration Patients

Age-Related Macular Degeneration: Epidemiology, Pathophysiology, Diagnosis, and Treatment

Pathophysiology of Age-Related Macular Degeneration: Implications for Treatment

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