TY - JOUR
T1 - Neutrophil extracellular traps in cardiac hypertrophy
T2 - a KLF2 perspective
AU - Riascos-Bernal, Dario F.
AU - Sibinga, Nicholas E.S.
N1 - Publisher Copyright:
© 2022, Riascos-Bernal et al.
PY - 2022/2/1
Y1 - 2022/2/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85124057773&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85124057773&partnerID=8YFLogxK
U2 - 10.1172/JCI156453
DO - 10.1172/JCI156453
M3 - Review article
C2 - 35104806
AN - SCOPUS:85124057773
SN - 0021-9738
VL - 132
JO - Journal of Clinical Investigation
JF - Journal of Clinical Investigation
IS - 3
M1 - e156453
ER -