Tear me down: Role of calpain in the development of cardiac ventricular hypertrophy

Cam Patterson, Andrea L. Portbury, Jonathan C. Schisler, Monte Willis

Research output: Contribution to journalReview article

37 Citations (Scopus)

Abstract

Cardiac hypertrophy develops most commonly in response to hypertension and is an independent risk factor for the development of heart failure. The mechanisms by which cardiac hypertrophy may be reversed to reduce this risk have not been fully determined to the point where mechanism-specific therapies have been developed. Recently, proteases in the calpain family have been implicated in the regulation of the development of cardiac hypertrophy in preclinical animal models. In this review, we summarize the molecular mechanisms by which calpain inhibition has been shown to modulate the development of cardiac (specifically ventricular) hypertrophy. The context within which calpain inhibition might be developed for therapeutic intervention of cardiac hypertrophy is then discussed.

Original languageEnglish (US)
Pages (from-to)453-462
Number of pages10
JournalCirculation research
Volume109
Issue number4
DOIs
StatePublished - Aug 5 2011
Externally publishedYes

Fingerprint

Calpain
Cardiomegaly
Tears
Hypertrophy
Peptide Hydrolases
Animal Models
Heart Failure
Hypertension
Therapeutics

Keywords

  • β3 integrin
  • calpain
  • calpastatin
  • cardiac hypertrophy
  • HSP90 heat-shock proteins
  • NF-κB inhibition

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Tear me down : Role of calpain in the development of cardiac ventricular hypertrophy. / Patterson, Cam; Portbury, Andrea L.; Schisler, Jonathan C.; Willis, Monte.

In: Circulation research, Vol. 109, No. 4, 05.08.2011, p. 453-462.

Research output: Contribution to journalReview article

Patterson, Cam ; Portbury, Andrea L. ; Schisler, Jonathan C. ; Willis, Monte. / Tear me down : Role of calpain in the development of cardiac ventricular hypertrophy. In: Circulation research. 2011 ; Vol. 109, No. 4. pp. 453-462.
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