Age-related focal loss of contractile vascular smooth muscle cells in retinal arterioles is accelerated by caveolin-1 deficiency.

Age-related focal loss of contractile vascular smooth muscle cells in retinal arterioles is accelerated by caveolin-1 deficiency.
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DOI:
10.1016/j.neurobiolaging.2018.06.039
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发表时间:
2018-11
影响因子:
4.2
通讯作者:
Elliott MH
Elliott MH
中科院分区:
医学2区
文献类型:
--
作者:
Reagan AM;Gu X;Paudel S;Ashpole NM;Zalles M;Sonntag WE;Ungvari Z;Csiszar A;Otalora L;Freeman WM;Stout MB;Elliott MH

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Cerebral microcirculation is critical for the preservation of brain health and vascular impairment is associated with age-related neurodegenerative diseases. Because the retina is a component of the central nervous system, cellular changes that occur in the aging retina are likely relevant to the aging brain and the retina provides the advantage that the entire vascular bed is visible, en face. In this study, we tested the hypothesis that normal, healthy aging alters the contractile vascular smooth muscle cell (VSMC) coverage of retinal arterioles. We found that aging results in a significant reduction of contractile VSMCs in focal patches along arterioles. Focal loss of contractile VSMCs occurs at a younger age in mice deficient in the senescence-associated protein, caveolin-1 (Cav-1). Age-related contractile VSMC loss is not exacerbated by genetic depletion of insulin-like growth factor-1 (IGF-1). The patchy loss of contractile VSMCs provides a cellular explanation for previous clinical studies showing focal microirregularities in retinal arteriolar responsiveness in healthy aged human subjects and is likely to contribute to age-related retinal vascular complications.
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