The role of calcifying nanoparticles in biology and medicine.

Calcifying nanoparticles (CNPs) (nanobacteria, nanobacteria-like particles, nanobes) were discovered over 25 years ago; nevertheless, their nature is still obscure. To date, nobody has been successful in credibly determining whether they are the smallest self-replicating life form on Earth, or whether they represent mineralo-protein complexes without any relation to living organisms. Proponents of both theories have a number of arguments in favor of the validity of their hypotheses. However, after epistemological analysis carried out in this review, all arguments used by proponents of the theory about the physicochemical model of CNP formation may be refuted on the basis of the performed investigations, and therefore published data suggest a biological nature of CNPs. The only obstacle to establish CNPs as living organisms is the absence of a fairly accurately sequenced genome at the present time. Moreover, it is clear that CNPs play an important role in etiopathogenesis of many diseases, and this association is independent from their nature. Consequently, emergence of CNPs in an organism is a pathological, not a physiological, process. The classification and new directions of further investigations devoted to the role of CNPs in biology and medicine are proposed.

Anticalcifying nanoparticle antibody titer is an independent risk factor for coronary artery calcification.

BACKGROUND: Calcium phosphate deposition is present even in the early phases of the atherosclerotic plaque formation. Calcifying nanoparticles (CNPs), previously known as nanobacteria, have emerged as a potential causative agent for pathological calcification in human vasculature. This study investigates the relationship between the anti-CNPs antibody titers and the extent of coronary calcification. METHODS: A total of 197 consecutive patients undergoing multidetector computed tomography were enrolled in this study. The patients with coronary artery calcification (CAC; n=103) were included in the CAC group, and those without calcification (n=94) were determined as controls. The commercially available enzyme-linked immunosorbent assay kits were used to detect IgG antibodies against CNPs in serum samples. RESULTS: Mean titers of anti-CNPs antibodies were higher in individuals with CAC than in the control group (0.4 ± 0.4 vs. 0.19 ± 0.21U; P<0.0001). Multivariate logistic regression analysis revealed that high anti-CNPs antibody levels were an independent correlate of CAC in addition to conventional risk factors such as age, hypertension, diabetes mellitus, and low levels of high-density lipoprotein cholesterol. When the CAC scores were subcategorized: score 0, 1-100, 101-400, and more than 400, they still correlated significantly with the anti-CNPs antibody, especially in the group having CAC scores greater than 400 (P<0.0001). CONCLUSION: Anti-CNPs antibodies are an independent risk factor for CAC and the antibody levels correlate with CAC scores.