ArticlePhysiological research2025
Cinacalcet Perturbs Membrane Permeability of bEND.3 Endothelial Cells and Suppresses Cell Proliferation.
Article in Physiological research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Exploring multiple drug actions of a CaNaunyn-Schmiedeberg's archives of pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca2+-sensing receptors (CaSR) are G-protein coupled receptors activated by elevated concentrations of extracellular Ca2+. Cinacalcet, a positive allosteric CaSR modulator, is used as a calcimimetic to inhibit parathyroid hormone release and thus lower serum Ca2+ in hypercalcemic patients. There is a recent trend of repurposing cinacalcet in multiple applications such as anti-cancer actions, treatment of diarrhea and prevention of kidney cyst formation. In this study we investigated whether cinacalcet inhibited proliferation of endothelial cells (EC). Inhibition of EC proliferation offers an anti-angiogenesis mechanism in suppressing tumor growth. Cinacalcet at >/=18 µM caused mitochondrial membrane depolarization, suppressed proliferation and induced apoptosis in mouse bEND.3 EC. In 2 mM Ca2+-containing bath solution, cinacalcet (>/=18 µM) caused an initial rise in [Ca2+]i followed by fura-2 leakage. Similar results were obtained in Ca2+-free or 4 mM Ca2+-containing bath solution. Cinacalcet-elicited Ca2+ signal was unaffected by NPS 2143, a negative allosteric modulator of CaSR. Cinacalcet also increased Ni2+ leakage and trypan blue uptake into cells. Cinacalcet-induced membrane leakiness and cytotoxicity did not appear to be related to membrane fluidity changes. These data suggest cinacalcet, in a manner independent of CaSR stimulation and membrane fluidity perturbation, caused membrane leakiness, eventually leading to inhibition of EC proliferation and EC death. Key words Ca2+-sensing receptors " Endothelium " Cinacalcet " Ca2+ " Membrane permeability.
Indexed as
Identifiers
41329537PMC12746853What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.