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Cell non-autonomous regulation of cerebrovascular aging processes by the somatotropic axis

Bickel, Marisa A., Csik, Boglarka, Gulej, Rafal, Ungvari, Anna, Nyul-Toth, Adam, Conley, Shannon M.·2023·Frontiers in Endocrinology
DOI 10.3389/fendo.2023.1087053
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Abstract

Age-related cerebrovascular pathologies, ranging from cerebromicrovascular functional and structural alterations to large vessel atherosclerosis, promote the genesis of vascular cognitive impairment and dementia (VCID) and exacerbate Alzheimer’s disease. Recent advances in geroscience, including results from studies on heterochronic parabiosis models, reinforce the hypothesis that cell non-autonomous mechanisms play a key role in regulating cerebrovascular aging processes. Growth hormone (GH) and insulin-like growth factor 1 (IGF-1) exert multifaceted vasoprotective effects and production of both hormones is significantly reduced in aging. This brief overview focuses on the role of age-related GH/IGF-1 deficiency in the development of cerebrovascular pathologies and VCID. It explores the mechanistic links among alterations in the somatotropic axis, specific macrovascular and microvascular pathologies (including capillary rarefaction, microhemorrhages, impaired endothelial regulation of cerebral blood flow, disruption of the blood brain barrier, decreased neurovascular coupling, and atherogenesis) and cognitive impairment. Improved understanding of cell non-autonomous mechanisms of vascular aging is crucial to identify targets for intervention to promote cerebrovascular and brain health in older adults.

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200 of 310 shown

Cited by

Metadata

Authors
Bickel, M. A., Csik, B., Gulej, R., Ungvari, A., Nyul-Toth, A., & Conley, S. M.
Venue
Frontiers in Endocrinology
Publisher
Frontiers Media SA
Published
2023-01-23
Volume
14
ISSN
1664-2392
DOI
10.3389/fendo.2023.1087053
Cited by
29
References
32
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • National Institutes of Health (R01AG070915, T32AG052363, 1P20GM125228)
  • American Heart Association (AHA83433, AHA916225)

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