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Calcium ions (Ca) act as important intracellular second messengers and play a key role in cellular physiological functions and signal transduction. Ca significantly affects the biological behavior of tumor cells by regulating mechanisms, such as cytoskeleton reorganization, cell migration, invasion, and immune escape. Although research on calcium homeostasis in tumor progression and metastasis was historically limited, it has recently received widespread attention. Growing evidence indicates that the disruption of calcium homeostasis is closely linked to the development, invasion, and metastasis of tumors. This paper systematically reviews the mechanisms governing calcium homeostasis in tumor progression and metastasis. We focused on calcium channels, pumps, and their regulatory roles in ionic signaling networks, the tumor microenvironment, downstream signaling pathways, and immune escape. We also discussed therapeutic strategies targeting tumor progression and metastasis via the modulation of calcium homeostasis. By elucidating the role of calcium homeostasis in tumor metastasis, this review aims to provide a theoretical foundation and to identify potential targets for novel anti-metastatic strategies.
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http://dx.doi.org/10.1016/j.canlet.2025.217908 | DOI Listing |
Acta Neuropathol Commun
September 2025
Department of Biomedical and Clinical Sciences and Department of Clinical Pathology, Linköping University, 58185, Linköping, Sweden.
Disruptions in synaptic transmission and plasticity are early hallmarks of Alzheimer's disease (AD). Endosomal trafficking, mediated by the retromer complex, is essential for intracellular protein sorting, including the regulation of amyloid precursor protein (APP) processing. The VPS35 subunit, a key cargo-recognition component of the retromer, has been implicated in neurodegenerative diseases, with mutations such as L625P linked to early-onset AD.
View Article and Find Full Text PDFNature
September 2025
Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA, USA.
As a key mitochondrial Ca transporter, NCLX regulates intracellular Ca signalling and vital mitochondrial processes. The importance of NCLX in cardiac and nervous-system physiology is reflected by acute heart failure and neurodegenerative disorders caused by its malfunction. Despite substantial advances in the field, the transport mechanisms of NCLX remain unclear.
View Article and Find Full Text PDFMech Ageing Dev
September 2025
Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Rome, Italy; Department of Medicine and Surgery, LUM University, Casamassima, Italy.
Age-related skeletal muscle decline is a major contributor to frailty, functional impairment, and loss of independence in advanced age. This process is characterized by selective atrophy of type II fibers, impaired excitation-contraction coupling, and reduced regenerative capacity. Emerging evidence implicates mitochondrial dysfunction as a central mechanism in the disruption of muscle homeostasis with age.
View Article and Find Full Text PDFExp Eye Res
September 2025
School of Basic Medicine, Qingdao University, Qingdao, Shandong Province, 266071, China; Department of Ophthalmology, Qingdao Eighth People's Hospital, Qingdao, Shandong Province, 266121, China; Institute of Stem Cell Regeneration Medicine, School of Basic Medicine, Qingdao University, Qingdao, Shan
Mitochondria play a crucial role in energy production and are intimately associated with ocular function. Mitochondrial dysfunction can trigger oxidative stress and inflammation, adversely affecting key ocular structures such as the lacrimal gland, lens, retina, and trabecular meshwork. This dysfunction may compromise the barrier properties of the trabecular meshwork, impeding aqueous humour outflow, elevating intraocular pressure, and resulting in optic nerve damage and primary open-angle glaucoma.
View Article and Find Full Text PDFReprod Toxicol
September 2025
Institute of Reproductive Medicine, Medical School, Nantong University, Nantong, Jiangsu 226019, China. Electronic address:
T-type calcium channels are pivotal in spermatogenesis. To evaluate the molecular mechanisms by which T-type calcium channels regulate spermatogenesis, we constructed animal and cellular models using T-type calcium channel inhibitor flunarizine (FNZ). Intraperitoneal administration of FNZ (30mg/kg) significantly impaired sperm motility, inhibited testicular germ cell proliferation, and disrupted sperm mitochondrial function in male mice.
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