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KLF4's role in regulating nitric oxide production and promoting microvascular formation following ischemic stroke
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DOI：10.1016/j.niox.2024.11.004.png)
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Abstract
En 中文
This study examines KLF4's role in endothelial cells (ECs), emphasizing its effects on nitric oxide (NO) production, microvascular formation, and oxidative stress regulation following ischemic stroke. Through highthroughput sequencing, we identified eight cell subpopulations in carotid artery tissues post-stroke, with KLF4 notably elevated in ECs. KLF4 overexpression in ECs promoted NO synthesis, enhanced endothelial tube formation, mitigated oxidative stress, and improved smooth muscle cells (SMCs) function, collectively boosting blood flow in ischemic regions. These findings highlight KLF4 as pivotal in vascular regeneration and oxidative stress reduction, positioning it as a promising target for cardiovascular and cerebrovascular therapies.
Keywords:
Ischemic stroke
Endothelial cells
KLF4
Microvascular formation
Carotid artery
Smooth muscle cells
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