2019
DOI: 10.21037/aes.2019.02.04
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The interplay between inflammation, immunity and commensal microflora in glaucomatous neurodegeneration

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Cited by 8 publications
(12 citation statements)
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“…In fact, it is more accurate to consider this glaucoma outcome as a consequence of both age-related stressors and as a neurological sensitivity to pressure, regardless of its magnitude [ 251 ]. As a matter of fact, this neurodegeneration in addition to IOP, is equally favored by other concomitant factors including the increase in glutamate levels, oxidative stress, mitochondria dysfunction and low grade inflammation [ 252 , 253 , 254 ].…”
Section: Neurodegeneration In Poagmentioning
confidence: 99%
“…In fact, it is more accurate to consider this glaucoma outcome as a consequence of both age-related stressors and as a neurological sensitivity to pressure, regardless of its magnitude [ 251 ]. As a matter of fact, this neurodegeneration in addition to IOP, is equally favored by other concomitant factors including the increase in glutamate levels, oxidative stress, mitochondria dysfunction and low grade inflammation [ 252 , 253 , 254 ].…”
Section: Neurodegeneration In Poagmentioning
confidence: 99%
“…Recently, work on the effects of microbiota on the intraocular pathology of glaucoma has accelerated, often focused on autoimmune or inflammatory aspects. Some of this work on glaucoma has been reviewed previously [14, 63-65], and may be divided into studies of oral microbiota and studies of gut microbiota, including gastric H . pylori colonization and gut microbiota-mediated autoimmunity to heat shock proteins (HSPs).…”
Section: Glaucomamentioning
confidence: 99%
“…There remains insufficient evidence to determine if a causative relationship exists, or if the observed association arises from shared susceptibility; subsequent studies on gut microbiota in POAG have taken the observed association with H . pylori infection as an indication that intestinal dysbiosis is a risk factor for both diseases [65].…”
Section: Glaucomamentioning
confidence: 99%
“…Hitzeschockfaktoren (HSF) sind im Zellkern lokalisiert und bilden durch Bindung an Hitzeschockelemente (HSE) eine komplexe Struktur im Promoterbereich des jeweiligen Gens. Dies führt zur Transkription von HSP, und die Stressreaktion wird primär durch HSF auf der transkriptionellen Ebene reguliert [374].…”
Section: Ausblickunclassified