Calcineurin Is a Universal Regulator of Vessel Function—Focus on Vascular Smooth Muscle Cells

Nolze, Alexander; Matern, Sebastian; Grossmann, Claudia

doi:10.3390/cells12182269

Cited by 3 publications

(1 citation statement)

References 181 publications

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“…Some of the genes in Table 1, only recently described as having a role in pathophysiology of CVD, were, e.g., PPP3CC-encoding calcineurin, an activator of transcription factor NFATC1. In pulmonary vascular smooth muscle cells, calcineurin/NFaT signaling was reported to regulate the release of Ca 2+ , resulting in increased vascular tone followed by pulmonary arterial hypertension [25]. In comparison, SPHK1 was involved in sepsis-induced inflammation [26].…”

Section: Outline Of Strategymentioning

confidence: 99%

Identification of Transcripts with Shared Roles in the Pathogenesis of Postmenopausal Osteoporosis and Cardiovascular Disease

Reppe,

Gundersen,

Sandve

et al. 2024

IJMS

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Epidemiological evidence suggests existing comorbidity between postmenopausal osteoporosis (OP) and cardiovascular disease (CVD), but identification of possible shared genes is lacking. The skeletal global transcriptomes were analyzed in trans-iliac bone biopsies (n = 84) from clinically well-characterized postmenopausal women (50 to 86 years) without clinical CVD using microchips and RNA sequencing. One thousand transcripts highly correlated with areal bone mineral density (aBMD) were further analyzed using bioinformatics, and common genes overlapping with CVD and associated biological mechanisms, pathways and functions were identified. Fifty genes (45 mRNAs, 5 miRNAs) were discovered with established roles in oxidative stress, inflammatory response, endothelial function, fibrosis, dyslipidemia and osteoblastogenesis/calcification. These pleiotropic genes with possible CVD comorbidity functions were also present in transcriptomes of microvascular endothelial cells and cardiomyocytes and were differentially expressed between healthy and osteoporotic women with fragility fractures. The results were supported by a genetic pleiotropy-informed conditional False Discovery Rate approach identifying any overlap in single nucleotide polymorphisms (SNPs) within several genes encoding aBMD- and CVD-associated transcripts. The study provides transcriptional and genomic evidence for genes of importance for both BMD regulation and CVD risk in a large collection of postmenopausal bone biopsies. Most of the transcripts identified in the CVD risk categories have no previously recognized roles in OP pathogenesis and provide novel avenues for exploring the mechanistic basis for the biological association between CVD and OP.

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Section: Outline Of Strategymentioning

confidence: 99%

Identification of Transcripts with Shared Roles in the Pathogenesis of Postmenopausal Osteoporosis and Cardiovascular Disease

Reppe,

Gundersen,

Sandve

et al. 2024

IJMS

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Efficacy and Safety Evaluation of Tacrolimus-Eluting Stent in a Porcine Coronary Artery Model

Park,

Na,

Jeong

et al. 2024

Tissue Eng Regen Med

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Ca2+ signaling in vascular smooth muscle and endothelial cells in blood vessel remodeling: a review

Suzuki,

Giles,

Zamponi

et al. 2024

Inflamm Regener

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Vascular smooth muscle cells (VSMCs) and endothelial cells (ECs) act together to regulate blood pressure and systemic blood flow by appropriately adjusting blood vessel diameter in response to biochemical or biomechanical stimuli. Ion channels that are expressed in these cells regulate membrane potential and cytosolic Ca2+ concentration ([Ca2+]cyt) in response to such stimuli. The subsets of these ion channels involved in Ca2+ signaling often form molecular complexes with intracellular molecules via scaffolding proteins. This allows Ca2+ signaling to be tightly controlled in localized areas within the cell, resulting in a balanced vascular tone. When hypertensive stimuli are applied to blood vessels for extended periods, gene expression in these vascular cells can change dramatically. For example, alteration in ion channel expression often induces electrical remodeling that produces a depolarization of the membrane potential and elevated [Ca2+]cyt. Coupled with endothelial dysfunction blood vessels undergo functional remodeling characterized by enhanced vasoconstriction. In addition, pathological challenges to vascular cells can induce inflammatory gene products that may promote leukocyte infiltration, in part through Ca2+-dependent pathways. Macrophages accumulating in the vascular adventitia promote fibrosis through extracellular matrix turnover, and cause structural remodeling of blood vessels. This functional and structural remodeling often leads to chronic hypertension affecting not only blood vessels, but also multiple organs including the brain, kidneys, and heart, thus increasing the risk of severe cardiovascular events. In this review, we outline recent advances in multidisciplinary research concerning Ca2+ signaling in VSMCs and ECs, with an emphasis on the mechanisms underlying functional and structural vascular remodeling.

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Calcineurin Is a Universal Regulator of Vessel Function—Focus on Vascular Smooth Muscle Cells

Cited by 3 publications

References 181 publications

Identification of Transcripts with Shared Roles in the Pathogenesis of Postmenopausal Osteoporosis and Cardiovascular Disease

Identification of Transcripts with Shared Roles in the Pathogenesis of Postmenopausal Osteoporosis and Cardiovascular Disease

Efficacy and Safety Evaluation of Tacrolimus-Eluting Stent in a Porcine Coronary Artery Model

Ca2+ signaling in vascular smooth muscle and endothelial cells in blood vessel remodeling: a review

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