Modulation of the monocyte/macrophage system in heart failure by targeting heme oxygenase-1.

Abstract:

:Upon myocardial infarction (MI) immune system becomes activated by extensive necrosis of cardiomyocytes releasing intracellular molecules called damage-associated molecular patterns. Overactive and prolonged immune responses are likely to be responsible for heart failure development and progression in patients surviving the ischemic episode. Heme oxygenase-1 (HO-1) plays a crucial role in heme degradation and in this way releases carbon monoxide, free iron, and biliverdin. This stress-inducible enzyme is induced by various oxidative and inflammatory signals. Consequently, biological actions of HO-1 are not limited to degradation of a toxic heme released from hemoproteins, but also provide an adaptive cellular response against chronic inflammation and oxidative injury. Indeed, the immunomodulatory and anti-inflammatory properties of HO-1 were demonstrated in several experimental studies, as well as in human cases of genetic HO-1 deficiency. HO-1 was shown to suppress the production, myocardial infiltration and inflammatory properties of monocytes and macrophages what resulted in limitation of post-MI cardiac damage. This review specifically addresses the role of HO-1, heme and its degradation products in macrophage biology and post-ischemic cardiac repair. A more complete understanding of these mechanisms is essential to develop new therapeutic approaches.

journal_name

Vascul Pharmacol

journal_title

Vascular pharmacology

authors

Tomczyk M,Kraszewska I,Dulak J,Jazwa-Kusior A

doi

10.1016/j.vph.2018.08.011

subject

Has Abstract

pub_date

2019-01-01 00:00:00

pages

79-90

eissn

1537-1891

issn

1879-3649

pii

S1537-1891(18)30115-0

journal_volume

112

pub_type

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