Biomineralization induced by stressed nanobacteria

Animal experiments provided direct evidence that myocyte apoptosis may be a causal mechanism of heart failure, suggesting that inhibition of this cell death process may constitute the basis for novel therapies. The data suggested that even inhibition of a small fraction of cardiac myocyte apoptosis could be instrumental in preventing cardiomyopathy. Here we analyze the mechanisms by which nanobacteria (NB) are expected to contribute to the inhibition of cellular functions in the heart. NB are protected by a nanocrystalline apatite shell. Under environmental stress, they produce a slime providing ideal conditions for individual mineralization and rapid formation of giant thrombogenic assemblies. We establish a model based upon a possible synergistic impact of physical and chemical stimuli on NB, exposing the principles of a novel preventive strategy promising to inhibit formation of NB clusters in the circulation.