Evidence map›Paper›PMID 15193035›Full record

ReviewBrain pathology (Zurich, Switzerland)2004

Cell death mechanisms following traumatic brain injury.

Ramesh Raghupathi

Open access · greenAbstract readComparative StudyReview
In one paragraph

Review in Brain pathology (Zurich, Switzerland), 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 247 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
247citing papers in PubMed, 1 pooled it
15.9field-weighted citation impact, top 1% 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

247 citing papers in PubMed, 1 synthesis or guideline pooled it, 549 citations in OpenAlex.

  1. Pooled it
  2. Development of an HInternational journal of molecular sciences · 2026
    Article
  3. Research progress on biomarkers of traumatic brain injury.Animal models and experimental medicine · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. The Role of Nanotechnology in Understanding the Pathophysiology of Traumatic Brain Injury.Central nervous system agents in medicinal chemistry · 2025
    Review
  19. Article
  20. Article

187 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Ramesh RaghupathiDrexel University College of Medicine, 2900 Queen Ln, Philadelphia, PA, USA. ramesh.raghupathi@drexel.edu
Drexel University · US

Funding

TRAUMATIC WHITE MATTER ABNORMALITIES OF HUMAN HEAD INJURYP50NS008803 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI GRADY, M SEAN · 1995 to 2005
$7.3M
Caspase mediated cell death after brain traumaR01NS041561 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI RAGHUPATHI, RAMESH · 2002 to 2006
$1.7M
SHORT TERM PHYSIOLOGIC EFFECTS OF THERAPYP01NS008803 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI GENNARELLI, THOMAS A · 1985 to 1994
–
NINDS NIH HHS NS08803NINDS NIH HHS NS41561
6 · The paper itself

Abstract

Neuronal and glial cell death and traumatic axonal injury contribute to the overall pathology of traumatic brain injury (TBI) in both humans and animals. In both head-injured humans and following experimental brain injury, dying neural cells exhibit either an apoptotic or a necrotic morphology. Apoptotic and necrotic neurons have been identified within contusions in the acute post-traumatic period, and in regions remote from the site of impact in the days and weeks after trauma, while degenerating oligodendrocytes and astrocytes have been observed within injured white matter tracts. We review and compare the regional and temporal patterns of apoptotic and necrotic cell death following TBI and the possible mechanisms underlying trauma-induced cell death. While excitatory amino acids, increases in intracellular calcium and free radicals can all cause cells to undergo apoptosis, in vitro studies have determined that neural cells can undergo apoptosis via many other pathways. It is generally accepted that a shift in the balance between pro- and anti-apoptotic protein factors towards the expression of proteins that promote death may be one mechanism underlying apoptotic cell death. The effect of TBI on cellular expression of survival promoting-proteins such as Bcl-2, Bcl-xL, and extracellular signal-regulated kinases, and death-inducing proteins such as Bax, c-Jun N-terminal kinase, tumor-suppressor gene, p53, and the calpain and caspase families of proteases are reviewed. In light of pharmacologic strategies that have been devised to reduce the extent of apoptotic cell death in animal models of TBI, our review also considers whether apoptosis may serve a protective role in the injured brain. Together, these observations suggest that cell death mechanisms may be representative of a continuum between apoptotic and necrotic pathways.

Indexed as

AnimalsBrain InjuriesCell DeathHumansNerve DegenerationNeurogliaNeurons

Identifiers

PMID15193035
PMCPMC8096005
OpenAlexW2084969905

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.