Role of Magnesium Deficiency in Promoting Atherosclerosis, Endothelial Dysfunction, and Arterial Stiffening as Risk Factors for Hypertension.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic literature without systematic search methodology or primary human data
PubMed 29891771 · doi:10.3390/ijms19061724
What was done
Narrative review synthesizing published mechanistic and physiological literature on the role of magnesium deficiency in the pathogenesis of endothelial dysfunction, atherosclerosis, arterial stiffening, and arterial hypertension.
What was found
The abstract reports no quantitative clinical data, sample sizes, or effect sizes. It details physiological mechanisms: magnesium serves as a calcium antagonist and promotes local vasodilators (prostacyclin, nitric oxide), whereas magnesium deficiency increases aldosterone production, vascular inflammation, and catecholamine-driven stress responses while decreasing antioxidant enzyme activity (glutathione peroxidase, superoxide dismutase, catalase) and antioxidant levels (vitamins C and E, selenium). Magnesium deficiency is also noted to alter collagen and elastin turnover and promote arterial calcification and stiffness.
Why it matters
It provides a consolidated conceptual model connecting cellular-level magnesium mechanisms to macrovascular dysfunction and hypertension risk.
Limits
As a narrative review, it lacks systematic search criteria, quality appraisal of cited evidence, and quantitative effect estimates. No clinical trial outcomes, human population details, or specific intake thresholds are provided in the abstract.
Cited by
- supports Magnesium lowers blood pressure by stimulating the production of prostacyclin and nitric oxide, which dilate blood vessels.