Evidence map›Paper›PMID 30755477›Full record

ArticleScience signaling2019

Inflammation, necrosis, and the kinase RIP3 are key mediators of AAG-dependent alkylation-induced retinal degeneration.

Mariacarmela Allocca, Joshua J Corrigan, Aprotim Mazumder, Kimberly R Fake, Leona D Samson

Open access · greenAbstract read
In one paragraph

Article in Science signaling, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 28% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. RIPK3 Contributes to Thyroid Hormone-Induced Photoreceptor Degeneration.International journal of molecular sciences · 2025
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. DNA Damage and Repair in Eye Diseases.International journal of molecular sciences · 2023
    Review
  12. Review
  13. Article
  14. Damage-Associated Molecular Patterns (DAMPs) in Retinal Disorders.International journal of molecular sciences · 2022
    Review
  15. The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

5 authors at 1 institution in 1 country.

Mariacarmela AlloccaDepartment of Biological Engineering, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.ORCID 0000-0001-6605-9863
Joshua J CorriganDepartment of Biological Engineering, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.
Aprotim MazumderDepartment of Biological Engineering, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.ORCID 0000-0002-3443-3010
Kimberly R FakeDepartment of Biological Engineering, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.
Leona D SamsonDepartment of Biological Engineering, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA. lsamson@mit.edu.ORCID 0000-0002-7112-1454
Center for Environmental Health · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI Paula T Hammond · 1985 to 2026
$93.9M
TOXICOLOGY CORE UNITP30ES002109 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI YAFFE, MICHAEL B · 1985 to 2020
$25.6M
IN VIVO ROLE OF DNA ALKYLATION REPAIRR01CA075576 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 1997 to 2011
$4.9M
EUKARYTIC DNA ALKYLATION REPAIRR01CA055042 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 1991 to 2010
$4.8M
NCI NIH HHS P30 CA014051NCI NIH HHS R01 CA055042NCI NIH HHS R01 CA075576NIEHS NIH HHS P30 ES002109
6 · The paper itself

Abstract

DNA-alkylating agents are commonly used to kill cancer cells, but the base excision repair (BER) pathway they trigger can also produce toxic intermediates that cause tissue damage, such as retinal degeneration (RD). Apoptosis, a process of programmed cell death, is assumed to be the main mechanism of this alkylation-induced photoreceptor (PR) cell death in RD. Here, we studied the involvement of necroptosis (another programmed cell death process) and inflammation in alkylation-induced RD. Male mice exposed to a methylating agent exhibited a reduced number of PR cell rows, active gliosis, and cytokine induction and macrophage infiltration in the retina. Dying PRs exhibited a necrotic morphology, increased 8-hydroxyguanosine abundance (an oxidative damage marker), and overexpression of the necroptosis-associated genes

Indexed as

DNA RepairAnimalsAntineoplastic Agents, AlkylatingApoptosisCell DeathDNA GlycosylasesFemaleInflammationMaleMice, 129 StrainMice, Inbred C57BLMice, KnockoutNecrosisPoly (ADP-Ribose) Polymerase-1Receptor-Interacting Protein Serine-Threonine KinasesRetinal Degeneration3-methyladenine-DNA glycosylaseAntineoplastic Agents, AlkylatingDNA GlycosylasesParp1 protein, mousePoly (ADP-Ribose) Polymerase-1Receptor-Interacting Protein Serine-Threonine KinasesRipk3 protein, mouse

Identifiers

PMID30755477
PMCPMC7150588
OpenAlexW2914548486

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.