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Updated: Jul 14, 2026
Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
Low-magnesium induces senescent features in cultured human endothelial cells
Silvia Ferrè1, Andrzej Mazur, Jeanette A M Maier
1University of Milan, Department of Preclinical Sciences-LITA Vialba, Milano, Italy.
Abstract:
Low magnesium (Mg) affects endothelial function, thus playing a role in cardiovascular diseases, including atherosclerosis. We here show that Mg deficiency acts through the induction of the pro-inflammatory cytokine interleukin (IL)-lalpha in cultured human endothelial cells. Indeed, the inhibition of IL-lalpha prevents low Mg-induced adhesion of monocytoid cells to the endothelium as well as the upregulation of the cdk inhibitor p21. We also demonstrate that Mg deficiency induces several features typically associated with endothelial senescence. While low Mg can affect gene expression at the transcriptional level, it also modulates the activity of the proteasome. Since endothelial senescence contributes to atherogenesis, our findings indicating that low Mg promotes senescence may shed some light on the molecular mechanisms linking Mg deficiency to cardiovascular diseases.
Insights
Low magnesium deficiency promotes endothelial senescence by increasing interleukin-1 alpha. This finding may explain how magnesium impacts cardiovascular diseases like atherosclerosis.
Area of Science:
- Endothelial biology
- Cardiovascular disease research
- Molecular mechanisms of aging
Background:
- Low magnesium (Mg) is linked to endothelial dysfunction and cardiovascular diseases.
- Endothelial senescence is a contributing factor to atherosclerosis development.
Purpose of the Study:
- To investigate the molecular mechanisms by which Mg deficiency affects endothelial cells.
- To determine if Mg deficiency induces endothelial senescence and its role in cardiovascular disease.
Main Methods:
- Cultured human endothelial cells were subjected to Mg deficiency.
- Interleukin-1 alpha (IL-1α) levels and monocytoid cell adhesion were measured.
- Expression of cell division cycle kinase (cdk) inhibitor p21 and senescence markers were assessed.
- Proteasome activity was analyzed under Mg deficiency.
Main Results:
- Mg deficiency induced pro-inflammatory interleukin-1 alpha (IL-1α) in endothelial cells.
- Inhibition of IL-1α prevented low Mg-induced monocytoid cell adhesion and p21 upregulation.
- Mg deficiency promoted features of endothelial senescence.
- Mg deficiency affected gene expression and modulated proteasome activity.
Conclusions:
- Mg deficiency promotes endothelial senescence via IL-1α induction.
- This senescence contributes to the molecular link between Mg deficiency and cardiovascular diseases like atherosclerosis.
- Understanding these mechanisms could inform strategies for preventing or treating Mg-related cardiovascular conditions.
