Key result
Continuous hypobaric hypoxia accelerates atherosclerotic plaque growth and instability in mice.
Why the study?
The effect of continuous hypobaric hypoxia, a major feature of high-altitude environment, on atherosclerosis progression has not been thoroughly investigated.
Does continuous hypobaric hypoxia promote atherosclerosis progression in ApoE -/- mice?
Does continuous hypobaric hypoxia promote atherosclerosis progression in ApoE -/- mice?
p-value: p=0.0017
Continuous hypobaric hypoxia, simulating high-altitude environments, accelerates atherosclerosis progression and plaque instability in a mouse model.
Does not support practice changes for hypoxic exposure; leaves open translation to human atherosclerosis.
Background: Intermittent normobaric hypoxia can promote the progression of atherosclerotic plaques.However, the effect of continuous hypobaric hypoxia (CHH), which is a major feature of high-altitude environment, on atherosclerosis has not been investigated thoroughly. Materials and Methods:After eight weeks of high-cholesterol diet, 30 male ApoE -/-mice were randomly divided into control and CHH groups.Mice in the CHH group lived in a hypobaric chamber with an oxygen content of 10% and air pressure of 364 mmhg (equal to 5,800 m altitude above sea level) for 4 weeks, while mice in the control group lived in normoxia condition.Then all mice were euthanized and the atherosclerotic lesion size and plaque stability in the aortic root were assessed.Intraplaque angiogenesis was characterized by immunostaining of CD31 and endomucin, which are identified as specific markers of vascular endothelial cells.Immunohistochemistry and qRT-PCR were performed to measure inflammatory cytokines.Results: Four weeks of CHH exposure promoted the growth of atherosclerotic lesions (p=0.0017) and decreased the stability of atherosclerotic plaques.In CHH group, plaque smooth muscle cells and collagen contents decreased, while plaque macrophages and lipids contents increased significantly (p<0.001).The contents of CD31 (p=0.0379) and endomucin (p=0.0196) in the plaque was higher in the CHH group and correlated with angiogenesis progression.Further, the content of monocyte chemotactic protein-1 (p=0.0376) and matrix metalloproteinase-2 was significantly higher (p=0.0212) in the CHH group. Conclusions: CHH may accelerate atherosclerosis progression in ApoE -/-mice by promoting angiogenesis and inflammation.
No takes yet. Share an insight, caveat, or question.
Luo et al. (2023) studied Atherosclerosis (n=30). Continuous hypobaric hypoxia vs. Normoxia was evaluated on Atherosclerotic lesion size (p=0.0017). Continuous hypobaric hypoxia exposure for 4 weeks significantly promoted the growth of atherosclerotic lesions (p=0.0017) and decreased plaque stability in ApoE-/- mice.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: