Calcium Signaling in Glomerular Cells
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".
Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 11068
Special Issue Editors
Interests: control of vascular reactivity by smooth muscle and endothelial cells and perivascular nerves; ion channels and GPCRs; acute kidney injury and chronic kidney disease; calcium signaling; renal oxidative stress; neonatal renal hemodynamics
Interests: ion channels and transporters in the kidney; glomerulus in health and disease; pathophysiology of cardiorenal syndrome
Special Issue Information
Dear Colleagues,
The glomerulus, a network of specialized blood capillaries in the kidney, plays a significant role in regulating homeostasis via selective filtration of plasma and solutes. Four major cell types maintain the structural integrity and functions of the glomerulus: 1) podocytes, the terminally differentiated visceral epithelial cells that make up the outer surface of the filtration barrier, 2) endothelial cells that line the capillaries, 3) mesangial cells that support the capillary loops and 4) parietal epithelial cells that line the inside of Bowman’s capsule. The physiological functions of the glomerulus require tight interplays and multi-directional cross-talks amongst the glomerular cells, alterations of which have been implicated in a wide range of pathologies manifest in progressive loss of renal function.
Glomerular cells express several ion channels, including small, intermediate, and large-conductance Ca2+-activated K+, transient receptor potential, Ca2+-activated Cl−, and voltage-dependent Ca2+ channels. These channels regulate Ca2+-dependent functions, including contractility, monolayer integrity, survival, and gene expression.
The mechanisms that underlie cytoskeletal dynamics in podocytes include regulated Ca2+ homeostasis, mainly via the canonical transient receptor potential (TRPC) channels. Alterations in Ca2+ signaling in podocytes have been linked to hereditary glomerulopathy and acquired proteinuric kidney disease. Similarly, pathological changes in Ca2+ signaling modalities and their downstream effectors have been proposed to be involved in glomerular endothelial dysfunction in severe diabetic kidney disease. Ca2+-dependent mesangial proliferation, apoptosis, and extracellular matrix accumulation contribute to the mechanisms that underlie glomerular derangement in disorders such as diabetes, multiple myeloma, IgA nephropathy, and lupus. However, the function and regulation of intracellular Ca2+ in Bowman’s capsule parietal epithelial cells are unclear.
Given the critical role of Ca2+-mediated signal transduction mechanisms in glomerular function and dysfunction, more rigorous investigations are necessary to improve the understanding of how the propagation of Ca2+-sensitive signaling cascades modulates glomerular cell structural and functional integrity in health and disease. Hence, this Special Issue will provide a platform for original regular research papers, short communications, and reviews on recent findings on ion channels and Ca2+ signaling in the glomerulus. The issue will encompass topics related to the structure, function, and regulation of Ca2+-permeable ion channels and their effectors in podocytes and glomerular endothelial, mesangial, and parietal epithelial cells.
Dr. Adebowale AdebiyiGuest Editor
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Keywords
- Podocytes
- Glomerular endothelial cells
- Mesangial cells
- Parietal epithelial cells
- Ca2+ signaling
- Ion channels
- Kidney disease
- Glomerulopathy
- Proliferation
- Cell death
- Gene transcription
- Cell cycle control
- Filtration barrier
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