Evidence map›Paper›PMID 25906154›Full record

ArticleCell death & disease2015

Macrophage- and RIP3-dependent inflammasome activation exacerbates retinal detachment-induced photoreceptor cell death.

K Kataoka, H Matsumoto, H Kaneko, S Notomi, K Takeuchi, J H Sweigard, A Atik, Y Murakami, K M Connor, H Terasaki and 2 more

Registry-linked trialOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03332758 (Inflammasomes in Cell Death in Macular Hole, Epiretinal Membrane, and Rhegmatogenous Retinal Detachment), which is not on this map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT03332758 completednot on this mapstarted 2017, after this paper: background citation

Inflammasomes in Cell Death in Macular Hole, Epiretinal Membrane, and Rhegmatogenous Retinal Detachment

TypeobservationalSponsorAllen C. Ho, MDRan2017 to 2018Enrolled41ConditionsRetinal Detachment, Full Thickness Macular Hole, Epiretinal MembraneArmsPars plana vitrectomy, External drainage
3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Pooled it
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  17. RIPK necrotic cell death pathway in both donor photoreceptor and host immune cells synergize to affect photoreceptor graft survival.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 2 countries.

K Kataoka1] Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, USA [2] Department of Ophthalmology, Nagoya University School of Medicine, Nagoya, Japan.
H MatsumotoAngiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, USA.
H KanekoDepartment of Ophthalmology, Nagoya University School of Medicine, Nagoya, Japan.
S NotomiAngiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, USA.
K TakeuchiAngiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, USA.
J H SweigardAngiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, USA.
A AtikAngiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, USA.
Y MurakamiAngiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, USA.
K M ConnorAngiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, USA.
H TerasakiDepartment of Ophthalmology, Nagoya University School of Medicine, Nagoya, Japan.
J W MillerAngiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, USA.
D G VavvasAngiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, USA.
Harvard University · USMassachusetts Eye and Ear Infirmary · USNagoya University · JP

Funding

P30 Core Grant for Vision ResearchP30EY014104 · NEI · MASSACHUSETTS EYE AND EAR INFIRMARY · PI Eric A Pierce · 2002 to 2026
$15.1M
Complement Mediated Neovascularization in RetinopathyR01EY022084 · NEI · MASSACHUSETTS EYE AND EAR INFIRMARY · PI CONNOR, KIP M · 2012 to 2015
$1.8M
Necroptosis and Neuroprotection in AMDR21EY023079 · NEI · MASSACHUSETTS EYE AND EAR INFIRMARY · PI VAVVAS, DEMETRIOS · 2013 to 2014
$404k
NEI NIH HHS EY014104NEI NIH HHS P30 EY014104NEI NIH HHS R01 EY022084NEI NIH HHS R01EY022084-01/S1NEI NIH HHS R21 EY023079NEI NIH HHS R21EY023079-01A1
6 · The paper itself

Abstract

Detachment of photoreceptors from the retinal pigment epithelium is seen in various retinal disorders, resulting in photoreceptor death and subsequent vision loss. Cell death results in the release of endogenous molecules that activate molecular platforms containing caspase-1, termed inflammasomes. Inflammasome activation in retinal diseases has been reported in some cases to be protective and in others to be detrimental, causing neuronal cell death. Moreover, the cellular source of inflammasomes in retinal disorders is not clear. Here, we demonstrate that patients with photoreceptor injury by retinal detachment (RD) have increased levels of cleaved IL-1β, an end product of inflammasome activation. In an animal model of RD, photoreceptor cell death led to activation of endogenous inflammasomes, and this activation was diminished by Rip3 deletion. The major source of Il1b expression was found to be infiltrating macrophages in the subretinal space, rather than dying photoreceptors. Inflammasome inhibition attenuated photoreceptor death after RD. Our data implicate the infiltrating macrophages as a source of damaging inflammasomes after photoreceptor detachment in a RIP3-dependent manner and suggest a novel therapeutic target for treatment of retinal diseases.

Indexed as

AgedAnimalsCell DeathFemaleHumansInflammasomesInterleukin-1betaMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutMiddle AgedPhotoreceptor Cells, VertebrateReceptor-Interacting Protein Serine-Threonine KinasesRetinal DetachmentInflammasomesInterleukin-1betaReceptor-Interacting Protein Serine-Threonine KinasesRIPK3 protein, humanRipk3 protein, mouse

Identifiers

PMID25906154
PMCPMC4650542
OpenAlexW2060672234

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.