Macrophages in Heart Failure with Reduced versus Preserved Ejection Fraction

被引：81

作者：

DeBerge, Matthew ^{[1
,2
]}

Shah, Sanjiv J. ^{[2
,3
]}

Wilsbacher, Lisa ^{[2
,3
]}

Thorp, Edward B. ^{[1
,2
]}

机构：

[1] Northwestern Univ, Dept Pathol, Feinberg Sch Med, Chicago, IL 60611 USA

[2] Northwestern Univ, Feinberg Sch Med, Feinberg Cardiovasc & Renal Res Inst, Chicago, IL 60611 USA

[3] Northwestern Univ, Dept Med, Feinberg Sch Med, Chicago, IL 60611 USA

来源：

TRENDS IN MOLECULAR MEDICINE | 2019年 / 25卷 / 04期

关键词：

ACUTE MYOCARDIAL-INFARCTION; RESIDENT CARDIAC MACROPHAGES; DIASTOLIC DYSFUNCTION; FIBROBLAST PRECURSORS; TYROSINE KINASE; GENE-EXPRESSION; STEADY-STATE; DOUBLE-BLIND; BONE-MARROW; INFLAMMATION;

D O I：

10.1016/j.molmed.2019.01.002

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

There is a growing number of individuals living with heart failure (HF) with reduced ejection fraction (HFrEF) or preserved ejection fraction (HFpEF). Long-term prognosis remains poor in both cases, especially in HFpEF, which is rising in incidence and lacks effective therapeutics. In both HFrEF and HFpEF, there is evidence that elevated inflammatory biomarkers, implicating innate immune cells such as macrophages, are associated with worsened clinical outcomes. Macrophage subsets are active in both inflammatory and reparative processes, yet our understanding of the causative roles for these cells in HF development and progression is incomplete. Here, we discuss recent findings interrogating the role of macrophages in inflammation and its resolution in the context of HF, with a specific focus on HFrEF versus HFpEF.

引用

页码：328 / 340

页数：13

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