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Calcium Dynamics in Disease: Mechanisms and Therapeutic Opportunities

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 31 March 2027 | Viewed by 477

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Guest Editor
Department of Science and Technological Innovation, Universita' degli Studi del Piemonte Orientale "Amedeo Avogadro", Alessandria, Italy
Interests: patch-clamp on neuroblastoma cell line with PFAS agents on GABA_A receptors; morphological and physiological alterations on rat testis and pancreas upon exposure to hypergravity; proteomics and metabolomics of monocytes exposed to inflammatory cytokines
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Special Issue Information

Dear Colleague,

Calcium ions (Ca2+) are paramount intracellular second messengers that control cellular pathways ranging from enzyme regulation, contractility, exocytosis, and synaptic activation to gene transcription. Ca2+ homeostasis is maintained by a sort of calcium toolkit that works through several players, such as membrane calcium channels, active pumps and exchangers, internal cellular stores, and metabotropic receptors. When calcium homeostasis fails, the cell becomes deregulated, leading to extremely variable diseases. Some of the most well-known neurodegenerative conditions, such as Parkinson’s disease and amyotrophic lateral sclerosis, are characterized by calcium overload and impaired cellular signaling, which culminates with cell death. Neuromuscular conditions, such as malignant hyperthermia, are often due to calcium channelopathies. Calcium deregulation drives heart arrhythmias or weak contractions and, at the vascular level, alters the wall tone, contributing to the onset of hypertension.

The role in cancer is even greater. Ca2+ is involved in cell proliferation and survival, and deregulated calcium-dependent pathways have profound effects on tumor onset and progression rate.

Last but not least, conditions deriving from altered extracellular calcium can be considered. Muscular weakness can be due to high calcium in extracellular fluids, with consequent nephrolithiasis, which can evolve into renal failure.

In summary, this Special Issue is open to shed light on the cellular and molecular mechanisms involved in the etiopathogenesis of calcium-dependent conditions and to identify putative and promising therapeutical approaches.

Dr. Valeria Magnelli
Guest Editor

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Keywords

  • calcium signaling
  • homeostasis
  • deregulation
  • calcium imbalance

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