Metabolic inflammation in heart failure with preserved ejection fraction

被引:142
|
作者
Schiattarella, Gabriele G. [1 ,2 ]
Rodolico, Daniele [3 ]
Hill, Joseph A. [1 ,4 ]
机构
[1] Univ Texas Southwestern Med Ctr Dallas, Dept Internal Med Cardiol, 6000 Harry Hines Blvd,NB11-208, Dallas, TX 75390 USA
[2] Univ Federico II, Dept Adv Biomed Sci, Via Pansini 5, I-80131 Naples, Italy
[3] Univ Cattolica Sacro Cuore, Dept Cardiovasc & Pulm Sci, Rome, Italy
[4] Univ Texas Southwestern Med Ctr Dallas, Dept Mol Biol, Dallas, TX 75390 USA
关键词
HFpEF; Inflammation; Obesity; Immunity; Metabolism; MYOCARDIAL SUBSTRATE METABOLISM; NITRIC-OXIDE; CARDIAC-FUNCTION; PHYSICAL-ACTIVITY; MACROPHAGE ACTIVATION; DIASTOLIC DYSFUNCTION; EXERCISE CAPACITY; ENERGY-METABOLISM; S-NITROSYLATION; IMMUNE-SYSTEM;
D O I
10.1093/cvr/cvaa217
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
One in 10 persons in the world aged 40 years and older will develop the syndrome of HFpEF (heart failure with preserved ejection fraction), the most common form of chronic cardiovascular disease for which no effective therapies are currently available. Metabolic disturbance and inflammatory burden contribute importantly to HFpEF pathogenesis. The interplay within these two biological processes is complex; indeed, it is now becoming clear that the notion of metabolic inflammation-metainflammation-must be considered central to HFpEF pathophysiology. Inflammation and metabolism interact over the course of syndrome progression, and likely impact HFpEF treatment and prevention. Here, we discuss evidence in support of a causal, mechanistic role of metainflammation in shaping HFpEF, proposing a framework in which metabolic comorbidities profoundly impact cardiac metabolism and inflammatory pathways in the syndrome.
引用
收藏
页码:423 / 434
页数:12
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