Long Noncoding RNA AF131217.1 Regulated Coronary Slow Flow-Induced Inflammation Affecting Coronary Slow Flow via KLF4

Jiang, Haibing; Ge, Zhengrong; Zhang, Lijing; Yang, Yi; Zhai, Xiaofeng; Chen, Zhanxi; Wei, Qing

doi:10.21470/1678-9741-2020-0573

Cited by 2 publications

References 22 publications

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Vascular mechanotransduction

Davis

Earley

et al. 2023

Physiological Reviews

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This review aims to survey the current state of mechanotransduction in vascular smooth muscle cells (VSMCs) and endothelial cells (ECs), including their sensing of mechanical stimuli and transduction of mechanical signals that result in the acute functional modulation and longer-term transcriptomic and epigenetic regulation of blood vessels. The mechanosensors discussed include ion channels, plasma membrane associated structures and receptors, and junction proteins. The mechanosignaling pathways presented include the cytoskeleton, integrins, extracellular matrix and intracellular signaling molecules. These are followed by discussions on mechanical regulation of transcriptome and epigenetics, relevance of mechanotransduction to health and disease, and interactions between ECs and VSMCs. Throughout this review, we offer suggestions for specific topics that require further understanding. In the closing section on Conclusions and Perspectives, we summarize what is known and point out the need to treat the vasculature as a system, including not only ECs and VSMCs, but also the extracellular matrix and other types of cells such as resident macrophages and pericytes, so that we can fully understand the physiology and pathophysiology of the blood vessel as a whole, thus enhancing the comprehension, diagnosis, treatment, and prevention of vascular diseases.

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Vascular mechanotransduction

Davis

Earley

et al. 2023

Physiological Reviews

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The protective effect of Iron Isomaltoside on myocardial ischemia-reperfusion injury via the suppression of KLF4/NF-κB signaling

Gong,

Zhao,

Zhang

et al. 2024

Preprint

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[Objectives] This study aimed to investigate the beneficial effects of iron isomaltoside (IIM) on myocardial function and the associated mechanisms in rats with myocardial ischemia/reperfusion (I/R)-induced damage and hypoxia/reoxygenation (H/R)-induced H9C2 cells. [Design & Methods] Changes in cardiac pathology after myocardial infarction (MI) were analyzed with hematoxylin-eosin staining. Myocardial cellapoptosis in the heart tissues of rats with MI was assessed using TUNEL staining. In H/R-induced H9C2 cells, cell viability and lactate dehydrogenase (LDH) and adenosine 5’-triphosphate levels were detected. Apoptosis and MMP in H9C2 cells were detected with flow cytometry. [Results] Our results demonstrated that IIM treatment reduced myocardial injury induced by ischemia-reperfusion (I/R) and suppressed cardiomyocyte apoptosis, inflammation, and autophagy induced by I/R in rats. Moreover, we confirmed that IIM repressed apoptosis and regulated MMP in H9C2 cells exposed to H/R. IIM relieved the inflammatory response and autophagy in H/R-treated H9C2 cells. In addition, IIM inhibited the Krüpple-like factor 4 (KLF4)/NF-κB pathway in H/R-induced H9C2 cells. Interestingly, the function of IIM on apoptosis, MMP, inflammation and autophagy were abolished by KLF4 overexpression in H/R-induced H9C2 cells. [Conclusions] In conclusion, IIM could repress cardiomyocyte apoptosis, inflammation and autophagy through the inhibition of the KLF4/NF-κB pathway and thus reduced myocardial injury in vivo and in vitro.

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Long Noncoding RNA AF131217.1 Regulated Coronary Slow Flow-Induced Inflammation Affecting Coronary Slow Flow via KLF4

Cited by 2 publications

References 22 publications

Vascular mechanotransduction

Vascular mechanotransduction

The protective effect of Iron Isomaltoside on myocardial ischemia-reperfusion injury via the suppression of KLF4/NF-κB signaling

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