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Role of NOD1 in Heart Failure Progression via Regulation of Ca2+ Handling.

Abstract：

BACKGROUND:Heart failure (HF) is a complex syndrome associated with a maladaptive innate immune system response that leads to deleterious cardiac remodeling. However, the underlying mechanisms of this syndrome are poorly understood. Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) is a newly recognized innate immune sensor involved in cardiovascular diseases. OBJECTIVES:This study evaluated the role of NOD1 in HF progression. METHODS:NOD1 was examined in human failing myocardium and in a post-myocardial infarction (PMI) HF model evaluated in wild-type (wt-PMI) and Nod1-/- mice (Nod1-/--PMI). RESULTS:The NOD1 pathway was up-regulated in human and murine failing myocardia. Compared with wt-PMI, hearts from Nod1-/--PMI mice had better cardiac function and attenuated structural remodeling. Ameliorated cardiac function in Nod1-/--PMI mice was associated with prevention of Ca2+ dynamic impairment linked to HF, including smaller and longer intracellular Ca2+ concentration transients and a lesser sarcoplasmic reticulum Ca2+ load due to a down-regulation of the sarcoplasmic reticulum Ca2+-adenosine triphosphatase pump and by augmented levels of the Na+/Ca2+ exchanger. Increased diastolic Ca2+ release in wt-PMI cardiomyocytes was related to hyperphosphorylation of ryanodine receptors, which was blunted in Nod1-/--PMI cardiomyocytes. Pharmacological blockade of NOD1 also prevented Ca2+ mishandling in wt-PMI mice. Nod1-/--PMI mice showed significantly fewer ventricular arrhythmias and lower mortality after isoproterenol administration. These effects were associated with lower aberrant systolic Ca2+ release and with a prevention of the hyperphosphorylation of ryanodine receptors under isoproterenol administration in Nod1-/--PMI mice. CONCLUSIONS:NOD1 modulated intracellular Ca2+ mishandling in HF, emerging as a new target for HF therapy.

journal_name

J Am Coll Cardiol

journal_title

Journal of the American College of Cardiology

authors

Val-Blasco A,Piedras MJGM,Ruiz-Hurtado G,Suarez N,Prieto P,Gonzalez-Ramos S,Gómez-Hurtado N,Delgado C,Pereira L,Benito G,Zaragoza C,Domenech N,Crespo-Leiro MG,Vasquez-Echeverri D,Nuñez G,Lopez-Collazo E,Boscá L,Fernánde

doi

10.1016/j.jacc.2016.10.073

subject

Has Abstract

pub_date

2017-01-31 00:00:00

pages

423-433

issue

4

eissn

0735-1097

issn

1558-3597

pii

S0735-1097(16)37135-2

journal_volume

69

pub_type

杂志文章

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