Evidence map›Paper›PMID 21383882›Full record

ArticleInternational journal of physiology, pathophysiology and pharmacology2009

Apoptosis, Bcl-2 family proteins and caspases: the ABCs of seizure-damage and epileptogenesis?

Tobias Engel, David C Henshall

Open access · greenAbstract read
In one paragraph

Article in International journal of physiology, pathophysiology and pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

54 citing papers in PubMed, 92 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Tobias EngelDepartment of Physiology & Medical Physics, Royal College of Surgeons in Ireland Dublin, Ireland.
David C Henshall
Royal College of Surgeons in Ireland · IE

Funding

MOLECULAR MECHANISMS OF SEIZURE INDUCED BRAIN INJURYR01NS039016 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SIMON, ROGER PANCOAST · 1999 to 2009
$2.6M
Caspases mediate seizure-induced brain injuryR01NS041935 · NINDS · EMANUEL HOSPITAL AND HEALTH CENTER · PI SIMON, ROGER PANCOAST · 2001 to 2004
$1.4M
Molecular determinants of epileptic bran injuryR01NS047622 · NINDS · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI SIMON, ROGER PANCOAST · 2005 to 2008
$1.4M
NINDS NIH HHS R01 NS039016NINDS NIH HHS R01 NS041935NINDS NIH HHS R01 NS047622Wellcome Trust
6 · The paper itself

Abstract

Epilepsy is a common, chronic neurological disorder. It is characterized by recurring seizures which are the result of abnormal electrical activity in the brain. Molecular pathways underlying neuronal death are of importance because prolonged seizure episodes (status epilepticus) cause significant damage to the brain, particularly within vulnerable structures such as the hippocampus. Additionally, repeated seizures over time in patients with poorly controlled epilepsy may cause further cell loss. Biochemical hallmarks associated with apoptosis have been identified in hippocampal and neocortical material removed from patients with pharmacoresistant epilepsy: altered expression of pro-apoptotic Bcl-2 family genes and increased expression of caspases and the presence of their cleaved forms. However, apoptotic cells are rarely detected in such patient material and there is evidence of anti-apoptotic signaling changes in the same tissue, including upregulation of Bcl-2 and Bcl-w. From animal studies there is evidence that both brief and prolonged seizures can cause neuronal apoptosis within the hippocampus. Such cell death can be associated with caspase and pro-apoptotic Bcl-2 family protein activation. Pharmacological or genetic modulations of these pathways can significantly influence DNA fragmentation and neuronal cell death after seizures. Thus, the signaling pathways associated with apoptosis are potentially important for the pathogenesis of epilepsy and may represent targets for neuroprotective and perhaps anti-epileptogenic therapies.

Identifiers

PMID21383882
PMCPMC3047241
OpenAlexW77755186

What OpenQuestion holds

Textmetadata
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.