Proliferative Pathways of Vascular Smooth Muscle Cells in Response to Intermittent Hypoxia

Kyotani, Yoji; Takasawa, Shin; Yoshizumi, Masanori

doi:10.3390/ijms20112706

Cited by 20 publications

(12 citation statements)

References 107 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Besides being produced by macrophages ( 35 ), IL-6 is also produced by a variety of different resident cells including keratinocytes, enterocytes, hepatocytes ( 33 ), pneumocytes, and bronchial epithelial cell ( 36 ), smooth muscle cells ( 37 ), skeletal muscle cells ( 38 ), osteoblasts ( 39 ), adipocytes ( 40 ), neurons ( 35 , 41 ). Interestingly IL-6 was also shown to be produced by lung epithelial cells in response to a variety of different stimuli including allergens, respiratory virus and exercise ( 42 – 44 ).…”

Section: The Il-6-cxcl10-macrophages Networkmentioning

confidence: 99%

Interleukin-6, CXCL10 and Infiltrating Macrophages in COVID-19-Related Cytokine Storm: Not One for All But All for One!

2021

View full text Add to dashboard Cite

SARS-COV-2 virus is responsible for the ongoing devastating pandemic. Since the early phase of the pandemic, the “cytokine-storm” appeared a peculiar aspect of SARS-COV-2 infection which, at least in the severe cases, is responsible for respiratory treat damage and subsequent multi-organ failure. The efforts made in the last few months elucidated that the cytokine-storm results from a complex network involving cytokines/chemokines/infiltrating-immune-cells which orchestrate the aberrant immune response in COVID-19. Clinical and experimental studies aimed at depicting a potential “immune signature” of SARS-COV-2, identified three main “actors,” namely the cytokine IL-6, the chemokine CXCL10 and the infiltrating immune cell type macrophages. Although other cytokines, chemokines and infiltrating immune cells are deeply involved and their role should not be neglected, based on currently available data, IL-6, CXCL10, and infiltrating macrophages could be considered prototype factors representing each component of the immune system. It rapidly became clear that a strong and continuous interplay among the three components of the immune response is mandatory in order to produce a severe clinical course of the disease. Indeed, while IL-6, CXCL10 and macrophages alone would not be able to fully drive the onset and maintenance of the cytokine-storm, the establishment of a IL-6/CXCL10/macrophages axis is crucial in driving the sequence of events characterizing this condition. The present review is specifically aimed at overviewing current evidences provided by both in vitro and in vivo studies addressing the issue of the interplay among IL-6, CXCL10 and macrophages in the onset and progression of cytokine storm. SARS-COV-2 infection and the “cytokine storm.”

show abstract

Section: The Il-6-cxcl10-macrophages Networkmentioning

confidence: 99%

Interleukin-6, CXCL10 and Infiltrating Macrophages in COVID-19-Related Cytokine Storm: Not One for All But All for One!

2021

View full text Add to dashboard Cite

show abstract

“…IH could cause not only pulmonary vascular disease but also systemic vascular diseases. In fact, Kyotani and his colleagues recently demonstrated that the epidermal growth factor family, such as epiregulin, amphiregulin, and neuregulin-1, and their receptor erbB2 were upregulated in vascular smooth muscle cells by IH [72], and these upregulations were mediated by the increase of IL-6 [73,74]. These findings indicate that IH seen in OSA patients modulates not only pulmonary but also systemic vascular pathophysiology.…”

Section: Effects Of Intermittent Hypoxia On Systemic Diseasesmentioning

confidence: 99%

Effects of Intermittent Hypoxia on Pulmonary Vascular and Systemic Diseases

Kimura

Ota

Kimura

et al. 2019

IJERPH

Self Cite

View full text Add to dashboard Cite

Obstructive sleep apnea (OSA) causes many systemic disorders via mechanisms related to sympathetic nerve activation, systemic inflammation, and oxidative stress. OSA typically shows repeated sleep apnea followed by hyperventilation, which results in intermittent hypoxia (IH). IH is associated with an increase in sympathetic activity, which is a well-known pathophysiological mechanism in hypertension and insulin resistance. In this review, we show the basic and clinical significance of IH from the viewpoint of not only systemic regulatory mechanisms focusing on pulmonary circulation, but also cellular mechanisms causing lifestyle-related diseases. First, we demonstrate how IH influences pulmonary circulation to cause pulmonary hypertension during sleep in association with sleep state-specific change in OSA. We also clarify how nocturnal IH activates circulating monocytes to accelerate the infiltration ability to vascular wall in OSA. Finally, the effects of IH on insulin secretion and insulin resistance are elucidated by using an in vitro chamber system that can mimic and manipulate IH. The obtained data implies that glucose-induced insulin secretion (GIS) in pancreatic β cells is significantly attenuated by IH, and that IH increases selenoprotein P, which is one of the hepatokines, as well as TNF-α, CCL-2, and resistin, members of adipokines, to induce insulin resistance via direct cellular mechanisms. Clinical and experimental findings concerning IH give us productive new knowledge of how lifestyle-related diseases and pulmonary hypertension develop during sleep.

show abstract

“…The involvement of these pathologies can lead to chronic diseases of multiple organs. A number of conditions may occur including atherosclerosis, cardiovascular disease, cerebrovascular disease, immunodeficiency, and metabolic abnormalities (pancreatic β cell dysfunction, insulin resistance, and increased free-fatty acid [FFA]) may occur [ 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of Intermittent Hypoxia on Cytokine Expression Involved in Insulin Resistance

Uchiyama

Ota

Ohbayashi

et al. 2021

IJMS

Self Cite

View full text Add to dashboard Cite

Sleep apnea syndrome (SAS) is a prevalent disorder characterized by recurrent apnea or hypoxia episodes leading to intermittent hypoxia (IH) and arousals during sleep. Currently, the relationship between SAS and metabolic diseases is being actively analyzed, and SAS is considered to be an independent risk factor for the development and progression of insulin resistance/type 2 diabetes (T2DM). Accumulating evidence suggests that the short cycles of decreased oxygen saturation and rapid reoxygenation, a typical feature of SAS, contribute to the development of glucose intolerance and insulin resistance. In addition to IH, several pathological conditions may also contribute to insulin resistance, including sympathetic nervous system hyperactivity, oxidative stress, vascular endothelial dysfunction, and the activation of inflammatory cytokines. However, the detailed mechanism by which IH induces insulin resistance in SAS patients has not been fully revealed. We have previously reported that IH stress may exacerbate insulin resistance/T2DM, especially in hepatocytes, adipocytes, and skeletal muscle cells, by causing abnormal cytokine expression/secretion from each cell. Adipose tissues, skeletal muscle, and the liver are the main endocrine organs producing hepatokines, adipokines, and myokines, respectively. In this review, we focus on the effect of IH on hepatokine, adipokine, and myokine expression.

show abstract

Proliferative Pathways of Vascular Smooth Muscle Cells in Response to Intermittent Hypoxia

Cited by 20 publications

References 107 publications

Interleukin-6, CXCL10 and Infiltrating Macrophages in COVID-19-Related Cytokine Storm: Not One for All But All for One!

Interleukin-6, CXCL10 and Infiltrating Macrophages in COVID-19-Related Cytokine Storm: Not One for All But All for One!

Effects of Intermittent Hypoxia on Pulmonary Vascular and Systemic Diseases

Effects of Intermittent Hypoxia on Cytokine Expression Involved in Insulin Resistance

Contact Info

Product

Resources

About