Evidence map›Paper›PMID 22581845›Full record

ReviewCardiovascular research2012

Calpains, mitochondria, and apoptosis.

Matthew A Smith, Rick G Schnellmann

Open access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed, 1 pooled it
9.7field-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

125 citing papers in PubMed, 1 synthesis or guideline pooled it, 237 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Baohuoside I CombatedAntioxidants (Basel, Switzerland) · 2026
    Article
  7. A systemic immunogenic reactor leveraging modifiedActa pharmaceutica Sinica. B · 2026
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Metal ions overloading and cell death.Cell biology and toxicology · 2024
    Review
  18. Article
  19. Review
  20. Article

65 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

2 authors at 1 institution in 1 country.

Matthew A SmithDepartment of Pharmaceutical and Biomedical Sciences, Center for Cell Death, Injury, and Regeneration, Medical University of South Carolina, 280 Calhoun Street, MSC140, Charleston, SC 29425, USA.
Rick G Schnellmann
Ralph H. Johnson VA Medical Center · US

Funding

Mitochondrial Biogenesis Promotes Recovery From Oxidant InjuryR01GM084147 · NIGMS · UNIVERSITY OF ARIZONA · PI SCHNELLMANN, RICK G · 2008 to 2016
$2.4M
MUSC FACIL EXPANSION &RENOV: SLE C06RR015455 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND, JOHN R · 2002 to 2002
$2.0M
MITOCHONDRIAL CALPAIN MEDIATED RENAL CELL DEATHR01ES012239 · NIEHS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI SCHNELLMANN, RICK G · 2004 to 2007
$1.1M
Training Program in Environmental Stress SignalingT32ES012878 · NIEHS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI SCHNELLMANN, RICK G · 2005 to 2010
$681k
NCRR NIH HHS C06 RR-015455NCRR NIH HHS C06 RR015455NIEHS NIH HHS ES-01223NIEHS NIH HHS R01 ES012239NIEHS NIH HHS T32 ES012878NIEHS NIH HHS T32ES012878-05NIGMS NIH HHS GM 084147NIGMS NIH HHS R01 GM084147
6 · The paper itself

Abstract

Mitochondrial activity is critical for efficient function of the cardiovascular system. In response to cardiovascular injury, mitochondrial dysfunction occurs and can lead to apoptosis and necrosis. Calpains are a 15-member family of Ca(2+)-activated cysteine proteases localized to the cytosol and mitochondria, and several have been shown to regulate apoptosis and necrosis. For example, in endothelial cells, Ca(2+) overload causes mitochondrial calpain 1 cleavage of the Na(+)/Ca(2+) exchanger leading to mitochondrial Ca(2+) accumulation. Also, activated calpain 1 cleaves Bid, inducing cytochrome c release and apoptosis. In renal cells, calpains 1 and 2 promote apoptosis and necrosis by cleaving cytoskeletal proteins, which increases plasma membrane permeability and cleavage of caspases. Calpain 10 cleaves electron transport chain proteins, causing decreased mitochondrial respiration and excessive activation, or inhibition of calpain 10 activity induces mitochondrial dysfunction and apoptosis. In cardiomyocytes, calpain 1 activates caspase 3 and poly-ADP ribose polymerase during tumour necrosis factor-α-induced apoptosis, and calpain 1 cleaves apoptosis-inducing factor after Ca(2+) overload. Many of these observations have been elucidated with calpain inhibitors, but most calpain inhibitors are not specific for calpains or a specific calpain family member, creating more questions. The following review will discuss how calpains affect mitochondrial function and apoptosis within the cardiovascular system.

Indexed as

ApoptosisAnimalsCalciumCalpainEndothelial CellsHumansKidneyMitochondriaMyocardiumMyocytes, Smooth MuscleCalciumCalpain

Identifiers

PMID22581845
PMCPMC3444233
OpenAlexW2047613950

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.