NMN and the Battle Against Vascular Calcification in Older Adults
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작성자 Wendell 작성일 25-09-22 19:33 조회 3 댓글 0본문
Aging brings many changes to the body, and one of the less discussed but significant issues is calcium buildup in blood vessels. This condition occurs when calcium deposits build up in the walls of arteries, making them stiff and less flexible. Over time, this can lead to high blood pressure, reduced blood flow, and an greater chance of myocardial infarction or cerebrovascular accident. Researchers are now exploring whether a molecule called NMN might play a role in potentially restoring vascular integrity.
NMN is a precursor to NAD+, a vital coenzyme found in every cell of the body. NAD+ concentrations decrease as we grow older, and this drop is linked to many age-related conditions, including dysfunctional cellular powerhouses and systemic inflammatory signaling. Both of these factors contribute to calcium deposition in vessel walls. By boosting the body’s NAD+ pool, NMN may help restore cellular energy production and mitigate reactive oxygen species, which are key drivers of ectopic calcification.
Recent studies in animal models have shown promising results. Mice given NMN oral dosing exhibited diminished calcified plaques in their arteries compared to placebo-treated animals. These animals also showed enhanced vascular compliance and improved endothelial performance. The proposed mechanism involves NMN’s ability to upregulate SIRT1 and related proteins, a family of proteins that regulate cellular health and longevity. Sirtuins help fine-tune phosphate and calcium signaling and inhibit osteogenic differentiation, a process visit that underlies arterial ossification.
In human studies, while robust clinical validation is pending, early trials suggest that NMN supplementation can improve markers of vascular health such as endothelial function and aortic rigidity. These are indirect but important indicators that the pathophysiological drivers of mineralization may be affected. Researchers are also investigating how NMN influences parallel degenerative processes, such as those involving chronic immune activation and cellular senescence, both of which are known to promote arterial aging.
Importantly, NMN is not a cure, nor is it a alternative to foundational care like regular movement, whole-food nutrition, and cardiovascular monitoring. However, it may serve as a adjunctive strategy to support vascular health as we age. Clinical trials are ongoing to determine the optimal dosage, long-term safety, and clinical efficacy across populations.
The science behind NMN and vascular calcification is still developing, but the preliminary data suggest meaningful potential. As our understanding of the molecular basis of senescence deepens, molecules like NMN may become part of a broader strategy to preserve vascular youth and function. For now, the focus remains on robust clinical investigation to establish causal relationships and ensure they translate safely into human health outcomes.
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