Vascular calcium signaling and aging

Research output: Contribution to journalJournal articlepeer-review

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Vascular calcium signaling and aging. / Harraz, Osama F; Jensen, Lars Jørn.

In: The Journal of Physiology, Vol. 599, No. 24, 2021, p. 5361-5377.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Harraz, OF & Jensen, LJ 2021, 'Vascular calcium signaling and aging', The Journal of Physiology, vol. 599, no. 24, pp. 5361-5377. https://doi.org/10.1113/JP280950

APA

Harraz, O. F., & Jensen, L. J. (2021). Vascular calcium signaling and aging. The Journal of Physiology, 599(24), 5361-5377. https://doi.org/10.1113/JP280950

Vancouver

Harraz OF, Jensen LJ. Vascular calcium signaling and aging. The Journal of Physiology. 2021;599(24):5361-5377. https://doi.org/10.1113/JP280950

Author

Harraz, Osama F ; Jensen, Lars Jørn. / Vascular calcium signaling and aging. In: The Journal of Physiology. 2021 ; Vol. 599, No. 24. pp. 5361-5377.

Bibtex

@article{7f46505c1bac4694a08b7c5bc9b0d10c,
title = "Vascular calcium signaling and aging",
abstract = "Changes in cellular Ca2+ levels have major influences on vascular function and blood pressure regulation. Vascular smooth muscle cells (SMCs) and endothelial cells (ECs) orchestrate vascular activity in distinct ways, often involving highly-specific fluctuations in Ca2+ signaling. Aging is a major risk factor for cardiovascular diseases, but the impact of aging per se on vascular Ca2+ signaling has received insufficient attention. We reviewed the literature for age-related changes in Ca2+ signaling in relation to vascular structure and function. Vascular tone dysregulation in several vascular beds has been linked to abnormal expression or activity of SMC voltage-gated Ca2+ channels, Ca2+-activated K+ channels or TRPC6 channels. Some of these effects were linked to altered caveolae density, microRNA expression, or 20-HETE abundance. Intracellular store Ca2+ handling was suppressed in aging mainly via reduced expression of intracellular Ca2+ release channels, and Ca2+ reuptake or efflux pumps. An increase in mitochondrial Ca2+ uptake, leading to oxidative stress, could also play a role in SMC hypercontractility and structural remodeling in aging. In ECs, aging entailed diverse effects on spontaneous and evoked Ca2+ transients, as well as structural changes at the EC-SMC interface. The concerted effects of altered Ca2+ signaling on myogenic tone, endothelium-dependent vasodilatation, and vascular structure are likely to contribute to blood pressure dysregulation and blood flow distribution deficits in critical organs. With the rise in the world aging population, future studies should be directed at solving specific aging-induced Ca2+ signaling deficits to combat the imminent accelerated vascular aging and increased risk of cardiovascular diseases.",
keywords = "Faculty of Health and Medical Sciences, Vascular smooth muscle, Endothelium, Aging, Calcium Signaling, vascular dysfunction, Hypertension, blood flow dysregulation",
author = "Harraz, {Osama F} and Jensen, {Lars J{\o}rn}",
year = "2021",
doi = "10.1113/JP280950",
language = "English",
volume = "599",
pages = "5361--5377",
journal = "The Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",
number = "24",

}

RIS

TY - JOUR

T1 - Vascular calcium signaling and aging

AU - Harraz, Osama F

AU - Jensen, Lars Jørn

PY - 2021

Y1 - 2021

N2 - Changes in cellular Ca2+ levels have major influences on vascular function and blood pressure regulation. Vascular smooth muscle cells (SMCs) and endothelial cells (ECs) orchestrate vascular activity in distinct ways, often involving highly-specific fluctuations in Ca2+ signaling. Aging is a major risk factor for cardiovascular diseases, but the impact of aging per se on vascular Ca2+ signaling has received insufficient attention. We reviewed the literature for age-related changes in Ca2+ signaling in relation to vascular structure and function. Vascular tone dysregulation in several vascular beds has been linked to abnormal expression or activity of SMC voltage-gated Ca2+ channels, Ca2+-activated K+ channels or TRPC6 channels. Some of these effects were linked to altered caveolae density, microRNA expression, or 20-HETE abundance. Intracellular store Ca2+ handling was suppressed in aging mainly via reduced expression of intracellular Ca2+ release channels, and Ca2+ reuptake or efflux pumps. An increase in mitochondrial Ca2+ uptake, leading to oxidative stress, could also play a role in SMC hypercontractility and structural remodeling in aging. In ECs, aging entailed diverse effects on spontaneous and evoked Ca2+ transients, as well as structural changes at the EC-SMC interface. The concerted effects of altered Ca2+ signaling on myogenic tone, endothelium-dependent vasodilatation, and vascular structure are likely to contribute to blood pressure dysregulation and blood flow distribution deficits in critical organs. With the rise in the world aging population, future studies should be directed at solving specific aging-induced Ca2+ signaling deficits to combat the imminent accelerated vascular aging and increased risk of cardiovascular diseases.

AB - Changes in cellular Ca2+ levels have major influences on vascular function and blood pressure regulation. Vascular smooth muscle cells (SMCs) and endothelial cells (ECs) orchestrate vascular activity in distinct ways, often involving highly-specific fluctuations in Ca2+ signaling. Aging is a major risk factor for cardiovascular diseases, but the impact of aging per se on vascular Ca2+ signaling has received insufficient attention. We reviewed the literature for age-related changes in Ca2+ signaling in relation to vascular structure and function. Vascular tone dysregulation in several vascular beds has been linked to abnormal expression or activity of SMC voltage-gated Ca2+ channels, Ca2+-activated K+ channels or TRPC6 channels. Some of these effects were linked to altered caveolae density, microRNA expression, or 20-HETE abundance. Intracellular store Ca2+ handling was suppressed in aging mainly via reduced expression of intracellular Ca2+ release channels, and Ca2+ reuptake or efflux pumps. An increase in mitochondrial Ca2+ uptake, leading to oxidative stress, could also play a role in SMC hypercontractility and structural remodeling in aging. In ECs, aging entailed diverse effects on spontaneous and evoked Ca2+ transients, as well as structural changes at the EC-SMC interface. The concerted effects of altered Ca2+ signaling on myogenic tone, endothelium-dependent vasodilatation, and vascular structure are likely to contribute to blood pressure dysregulation and blood flow distribution deficits in critical organs. With the rise in the world aging population, future studies should be directed at solving specific aging-induced Ca2+ signaling deficits to combat the imminent accelerated vascular aging and increased risk of cardiovascular diseases.

KW - Faculty of Health and Medical Sciences

KW - Vascular smooth muscle

KW - Endothelium

KW - Aging

KW - Calcium Signaling

KW - vascular dysfunction

KW - Hypertension

KW - blood flow dysregulation

U2 - 10.1113/JP280950

DO - 10.1113/JP280950

M3 - Journal article

C2 - 34705288

VL - 599

SP - 5361

EP - 5377

JO - The Journal of Physiology

JF - The Journal of Physiology

SN - 0022-3751

IS - 24

ER -

ID: 282743223