2015
DOI: 10.1016/j.jacc.2015.04.064
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Heme Oxygenase-1 Gene Therapy Provides Cardioprotection Via Control of Post-Ischemic Inflammation

Abstract: Whereas HO-1 deficiency exacerbates post-ischemic cardiac inflammation in mice, hHO-1 gene therapy attenuates inflammation after ischemia and reperfusion in murine and porcine hearts. Regional hHO-1 gene therapy provides cardioprotection in a pre-clinical porcine ischemia/reperfusion model.

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Cited by 69 publications
(55 citation statements)
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“…Accumulating studies indicated that both mice and human deficiency in HO-1 expression have a phenotype of increased inflammatory state [24]. As an active component extracted from Polygonum multiflorum, TSG showed obvious protection effects in a series of diseases.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Accumulating studies indicated that both mice and human deficiency in HO-1 expression have a phenotype of increased inflammatory state [24]. As an active component extracted from Polygonum multiflorum, TSG showed obvious protection effects in a series of diseases.…”
Section: Discussionmentioning
confidence: 99%
“…Recent research demonstrated that overexpression of HO-1 markedly suppressed TNF- α inducing airway inflammation by inhibition of oxidative stress [23]. Moreover, animal models with HO-1 deficiency were susceptible to severe inflammation [24, 25], while the role of HO-1 in TSG inducing anti-inflammatory property has not been evaluated yet.…”
Section: Introductionmentioning
confidence: 99%
“…In contrast, transgenic animals with cardiac-specific Hmox1 overexpression were better protected from I/R, with improved contractile recovery and reduced infarct size, inflammatory cell infiltration, oxidative damage, and apoptosis [54]. Recently, Hmox1 gene transfer was shown to attenuate post-ischemic inflammation in both murine and porcine I/R-injured hearts [22]. In addition, beneficial effects of Hmox1 were demonstrated also under prolonged ischemia in mice with permanent ligation of the coronary artery [47].…”
Section: Introductionmentioning
confidence: 99%
“…For instance, dexamethasone is a potent glucocorticoid with anti-inflammatory effects and can protect ischemic cardiomyocytes from apoptosis. Heme oxygenase-1 (HO-1), induced by stress and inflammation can also protect ischemic cardiomyocytes from apoptosis [20,21]. One group synthesized dexamethasone-conjugated polyethylenimine (PEI-Dexa) as an anti-apoptotic gene carrier to deliver plasmid encoding HO-1 into injured H9C2 rat cardiomyocytes [20].…”
Section: Augmenting Cytoprotective Mechanismsmentioning
confidence: 99%