Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-4-15
pubmed:abstractText
Ongoing advances in vector technology, cardiac gene delivery, and, most importantly, our understanding of HF pathogenesis, encourage consideration of gene therapy for HF at this time. At the present time, strategies that enhance sarcoplasmic calcium transport are supported by substantial evidence in both cardiomyocytes derived from patients with HF and in animal models. In addition, efforts to promote cardiomyocyte survival and function through modulation of antiapoptotic signaling appear quite promising. In ongoing efforts to target cardiac dysfunction, gene transfer provides an important tool to improve our understanding of the relative contribution of specific pathways. Through such experiments, molecular targets can be validated for therapeutic intervention, whether pharmacologic or genetic. Translating these basic investigations into clinical gene therapy for HF, however, remains a formidable challenge. Further development of concepts established in rodent models will be required in large animal models with clinical grade vectors and delivery systems to evaluate both efficacy and safety of these approaches. Nevertheless, practical advances and our growing understanding of the molecular pathogenesis of HF provide reason for cautious optimism.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0025-7125
pubmed:author
pubmed:issnType
Print
pubmed:volume
87
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
553-67
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Genetic editing of dysfunctional myocardium.
pubmed:affiliation
Massachusetts General Hospital, Boston, MA, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't