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

Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia (IH) and is a risk factor for cardiovascular diseases (e.g., atherosclerosis) and chronic inflammatory diseases (CID). The excessive proliferation of vascular smooth muscle cells (VSMCs) plays a pivotal role in the progression of atherosclerosis. Hypoxia-inducible factor-1 and nuclear factor-κB are thought to be the main factors involved in responses to IH and in regulating adaptations or inflammation pathways, however, further evidence is needed to demonstrate the underlying mechanisms of this process in VSMCs. Furthermore, few studies of IH have examined smooth muscle cell responses. Our previous studies demonstrated that increased interleukin (IL)-6, epidermal growth factor family ligands, and erbB2 receptor, some of which amplify inflammation and, consequently, induce CID, were induced by IH and were involved in the proliferation of VSMCs. Since IH increased IL-6 and epiregulin expression in VSMCs, the same phenomenon may also occur in other smooth muscle cells, and, consequently, may be related to the incidence or progression of several diseases. In the present review, we describe how IH can induce the excessive proliferation of VSMCs and we develop the suggestion that other CID may be related to the effects of IH on other smooth muscle cells.

Medienart:

E-Artikel

Erscheinungsjahr:

2019

Erschienen:

2019

Enthalten in:

Zur Gesamtaufnahme - volume:20

Enthalten in:

International journal of molecular sciences - 20(2019), 11 vom: 01. Juni

Sprache:

Englisch

Beteiligte Personen:

Kyotani, Yoji [VerfasserIn]
Takasawa, Shin [VerfasserIn]
Yoshizumi, Masanori [VerfasserIn]

Links:

Volltext

Themen:

Biomarkers
Epiregulin
Interleukin
Interleukins
Intermittent hypoxia
Journal Article
Reactive Oxygen Species
Review
Transcription Factors
Vascular smooth muscle cells

Anmerkungen:

Date Completed 20.11.2019

Date Revised 25.02.2020

published: Electronic

Citation Status MEDLINE

doi:

10.3390/ijms20112706

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM297769715