Zinc-dependent mechanisms of reparative regeneration: theoretical aspects and translational perspectives

Zinc is an essential component of more than 10% of the human proteome and serves as a cofactor for nearly 300 metalloenzymes. Interaction with zinc regulates protein activity and influences numerous intracellular processes, whereas removal of zinc from an enzyme results in complete loss of its enzymatic activity. Thus, zinc functions as an intracellular signaling molecule at all levels of signal transduction, affecting multiple metabolic pathways. Reparative regeneration is a cascade mechanism for restoring cells and tissues lost due to pathological processes. Understanding the molecular mechanisms of reparative regeneration is crucial for developing clinical strategies to enhance tissue repair capacity. Zinc plays a key role in reparative regeneration. Modulation of zinc-dependent signaling pathways represents a promising approach in experimental pharmacology. Novel Russian zinc complexes with N-alkenylimidazoles have demonstrated efficacy as pharmacologic agents in correcting a wide range of pathological conditions associated with reparative regeneration. These compounds have shown antihypoxic, antioxidant, wound-healing, anti-inflammatory, antiulcer, and analgesic effects. Their safety and high bioavailability offer broad translational potential. Wound healing is a complex and evolving process involving multiple cell types, including immune cells. These cells secrete cytokines and growth factors that contribute to the amplification of inflammation. This review provides a contemporary overview of zinc-dependent intracellular and systemic processes and highlights possible mechanisms of action of zinc complexes within the molecular and cellular pathways of reparative regeneration.