We develop, conduct clinical trials and introduce into the clinic new methods of influencing the extracellular matrix.
CHELILATION
Accumulation of macromolecular damage (especially in extracellular matrix (ECM) protein, nuclear pore complex (NPC) protein and histones) is a concomitant feature of aging. Stochastic non-enzymatic modifications of the ECM trigger cellular senescence, as well as many other signs of aging that are characteristic of the composition of organic barriers and lead to tissue fibrosis. This makes the extracellular matrix a key target for interventions.
One of the most effective methods for assessing organ and tissue retention of heavy metals is to compare urinary heavy metal levels before and after administration of a pharmaceutical chelating agent such as EDTA, DMSA, or DMPS. Therefore, we always conduct a study (analysis) of urine and blood in dynamics after chelation therapy.
The accumulation of damage in macromolecules (especially extracellular matrix (ECM) proteins, nuclear pore complex (NPC) proteins and histones) is a concomitant feature of aging. Stochastic non-enzymatic modifications of the ECM trigger cellular senescence, and many other signs of aging affect the integrity of organ barriers and lead to tissue fibrosis. This makes the extracellular matrix a key target for interventions. The most promising correction strategies may be AGE inhibitors (chelators, compounds of the O-acetyl group or compounds with transglycation activity, amadorins and amadoriases), glucose degrading agents, elastogenesis stimulants and RAGE antagonists.
