Neurovascular dysfunction in glaucoma

Alarcon-Martinez, Luis; Shiga, Yukihiro; Villafranca-Baughman, Deborah; Cueva Vargas, Jorge L.; Vidal Paredes, Isaac A.; Quintero, Heberto; Fortune, Brad; Danesh-Meyer, Helen; Di Polo, Adriana

doi:10.1016/j.preteyeres.2023.101217

Cited by 19 publications

(5 citation statements)

References 462 publications

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“…When NVU physiological function is normal, the unit senses regional mechanical stress, neurotransmitters released by neurons, or other types of biological signals, and transmits electrochemical signals to nearby blood vessels or glial cells that trigger the downstream biological responses. The interaction between neurons, glial cells, and blood vessels within the NVU is crucial; any abnormality in these components can disrupt the microenvironment's homeostasis [23]. In this section, we discuss the cellular and molecular mechanisms of the NVU and their pathophysiological implications in glaucoma and how the function is altered with glaucomatous optic neuropathy.…”

Section: Basic Research Of "Dual-pressure Theory"mentioning

confidence: 99%

“Dual‐pressure theory” in pathogenesis of glaucomatous optic neuropathy from the Beijing intracranial and intraocular pressure study

Cheng,

Yusufu,

Weinreb

et al. 2024

Eye & ENT Research

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The mechanical theory of glaucoma indicates that high intraocular pressure (IOP) leads to glaucomatous optic nerve damage. However, nearly half of primary open‐angle glaucoma patients with normal intraocular pressure also exhibit progression of what appears to be glaucomatous optic nerve damage. Our earlier prospective study identified for the first time that the relatively low intracranial pressure (ICP) is also an important risk factor for progressive glaucomatous injury of normal‐tension glaucoma. When considering the results of studies in nonhuman primates, clinical research, large‐scale natural‐population studies, and basic laboratory investigations, a new understanding of the pathophysiology of glaucoma, the “Dual‐Pressure Theory”, has been proposed. This theory states that “either high IOP or low ICP contributes to increasing the translaminar cribrosa pressure difference; it is the pressure difference rather than the IOP alone that results in the glaucomatous optic neuropathy”. Here, we provide a systematic introduction to Dual‐Pressure Theory relating to glaucoma, the form of a research map, an outline of basic laboratory investigations, the main methodology, and research updates.

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Section: Basic Research Of "Dual-pressure Theory"mentioning

confidence: 99%

“Dual‐pressure theory” in pathogenesis of glaucomatous optic neuropathy from the Beijing intracranial and intraocular pressure study

Cheng,

Yusufu,

Weinreb

et al. 2024

Eye & ENT Research

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“…138 Increased intraocular pressure in the eye causes damage to IP-TNTs that impairs the blood flow and represents a risk factor for the development of glaucoma. 139,140 An important metabolic aspect of interactions between PCs and ECs was revealed recently. 31 ECs are highly glycolytic and the larger part of lactate that is produced is secreted into the ECM making the lactate available for uptake by PCs.…”

Section: Pericytes As Therapeutic Targets In Pathological Angiogenesismentioning

confidence: 99%

“… 138 Increased intraocular pressure in the eye causes damage to IP-TNTs that impairs the blood flow and represents a risk factor for the development of glaucoma. 139 , 140 …”

Section: Pericytes As Therapeutic Targets In Pathological Angiogenesismentioning

confidence: 99%

New Insights in ATP Synthesis as Therapeutic Target in Cancer and Angiogenic Ocular Diseases

van Noorden,

Yetkin-Arik,

Serrano Martinez

et al. 2024

J Histochem Cytochem.

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Lactate and ATP formation by aerobic glycolysis, the Warburg effect, is considered a hallmark of cancer. During angiogenesis in non-cancerous tissue, proliferating stalk endothelial cells (ECs) also produce lactate and ATP by aerobic glycolysis. In fact, all proliferating cells, both non-cancer and cancer cells, need lactate for the biosynthesis of building blocks for cell growth and tissue expansion. Moreover, both non-proliferating cancer stem cells in tumors and leader tip ECs during angiogenesis rely on glycolysis for pyruvate production, which is used for ATP synthesis in mitochondria through oxidative phosphorylation (OXPHOS). Therefore, aerobic glycolysis is not a specific hallmark of cancer but rather a hallmark of proliferating cells and limits its utility in cancer therapy. However, local treatment of angiogenic eye conditions with inhibitors of glycolysis may be a safe therapeutic option that warrants experimental investigation. Most types of cells in the eye such as photoreceptors and pericytes use OXPHOS for ATP production, whereas proliferating angiogenic stalk ECs rely on glycolysis for lactate and ATP production. (J Histochem Cytochem XX.XXX–XXX, XXXX)

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“…Many studies promote the role of vascular abnormalities in glaucomatous damage [ 4 , 5 ]. According to this hypothesis, reduced perfusion pressure, deficient vascular autoregulation and loss of neurovascular coupling can lead to damage of the optic nerve head [ 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 ]. Abnormality in vascular function also influences the secretion and drainage of aqueous humour, consequently increasing IOP and contributing to the pathogenesis and progression of glaucoma [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Glaucoma, Pseudoexfoliation and Hearing Loss: A Systematic Literature Review

Meliante,

Piccotti,

Tanga

et al. 2024

JCM

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Purpose: To investigate the relationship between glaucoma, pseudoexfoliation and hearing loss (HL). Methods: A systematic literature search following PRISMA guidelines was conducted using the PubMed, Embase, Scopus and Cochrane databases from 1995 up to 28 August 2023. Results: Thirty studies out of the 520 records screened met the inclusion criteria and were included. Most articles (n = 20) analysed the association between pseudoexfoliation syndrome (XFS) and HL, showing XFS patients to have higher prevalence of sensorineural hearing loss (SNHL) at both speech frequencies (0.25, 0.5, 1 and 2 kHz), and higher frequencies (4 and 8 kHz) compared to controls in most cases. No significant differences in prevalence or level of HL between XFS and pseudoexfoliative glaucoma (XFG) were detected in most studies. Eight articles analysed the relationship between primary open-angle glaucoma (POAG) and HL. Overall, a positive association between the two conditions was highlighted across all studies except for two cases. Similarly, articles focusing on NTG and HL (n = 4) showed a positive association in most cases. The role of autoimmunity and, in particular, the presence of antiphosphatidylserine antibodies (APSA) in patients with NTG and HL suggested an underlying autoimmune or vascular mechanism contributing to their pathogenesis. Only one study analysed the relationship between angle-closure glaucoma (ACG) and HL, showing higher incidence of ACG in patients with SNHL compared to normal hearing controls. Conclusions: Most studies detected an association between XFS and HL as well as POAG/NTG/ACG and HL, suggesting the presence of a similar pathophysiology of neurodegeneration. However, given the strength of the association of XFS with HL, it remains unclear whether the presence of XFG is further associated with SNHL. Further research specifically targeted to assess the correlation between glaucoma, XFS and HL is warranted to provide a more comprehensive understanding of this association.

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Neurovascular dysfunction in glaucoma

Cited by 19 publications

References 462 publications

“Dual‐pressure theory” in pathogenesis of glaucomatous optic neuropathy from the Beijing intracranial and intraocular pressure study

“Dual‐pressure theory” in pathogenesis of glaucomatous optic neuropathy from the Beijing intracranial and intraocular pressure study

New Insights in ATP Synthesis as Therapeutic Target in Cancer and Angiogenic Ocular Diseases

Glaucoma, Pseudoexfoliation and Hearing Loss: A Systematic Literature Review

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