Neutrophil extracellular traps in cardiac hypertrophy: a KLF2 perspective.
Neutrophil extracellular traps in cardiac hypertrophy: a KLF2 perspective.
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DOI：
10.1172/jci156453
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发表时间：
2022-02-01
期刊：
影响因子：
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通讯作者：
Sibinga NE
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文献类型：
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作者：
Riascos-Bernal DF;Sibinga NE
美国约有600万成年人患有心力衰竭，诊断后5年的死亡率仍高达约50%。对疾病发病机制的不完全理解限制了治疗，特别是在射血分数保留的心力衰竭的情况下，这种情况通常与心脏肥大相关。中性粒细胞是血液中最丰富的白细胞，具有抗菌活性以外的功能，并参与无菌性炎症和疾病;然而，它们在非缺血性心脏肥大和心力衰竭中的作用尚不清楚。在这一期的JCI中，Tang等人在血管紧张素II诱导的心肌病小鼠模型中表明，中性粒细胞胞外陷阱（NET）的形成有助于心脏肥大和功能障碍，而Krüppel样因子2（KLF 2）在中性粒细胞中起对抗这一过程的作用。是否一个以心脏肥大和心力衰竭患者为中心的策略可能有益值得进一步研究。
About 6 million adults in the United States have heart failure, and the mortality five years after diagnosis remains high at approximately 50%. Incomplete understanding of disease pathogenesis limits therapeutics, especially in the case of heart failure with preserved ejection fraction, a condition commonly associated with cardiac hypertrophy. Neutrophils, the most abundant leukocyte in blood, have functions beyond antimicrobial activity and participate in both sterile inflammation and disease; however, their role in nonischemic cardiac hypertrophy and heart failure is underexplored. In this issue of the JCI, Tang et al. show that neutrophil extracellular trap (NET) formation contributes to cardiac hypertrophy and dysfunction in a mouse model of angiotensin II–induced cardiomyopathy, and that Krüppel-like factor 2 (KLF2) functions in neutrophils to oppose this process. Whether a neutrophil-centered strategy may benefit patients with cardiac hypertrophy and failure deserves further investigation.