REVIEW: Modified N-Terminal Fragments of Galanin: Cardioprotective Properties and Mechanisms of Action

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Oleg I. Pisarenko^1,a*, Irina M. Studneva¹, and Oxana M. Veselova¹

¹National Medical Research Center for Cardiology, 121552 Moscow, Russia

^* To whom correspondence should be addressed.

Received July 28, 2021; Revised August 15, 2021; Accepted August 16, 2021

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The design of new drugs for treatment of cardiovascular diseases based on endogenous peptide hormones is of undoubted interest and stimulates intensive experimental research. One of the approaches for development in this area is synthesis of the short bioactive peptides that mimic effects of the larger peptide molecules and have improved physicochemical characteristics. In recent years, it has been found that the N-terminal fragments of the neuropeptide galanin reduce metabolic and functional disorders in the experimental heart damage. The review presents literature data and generalized results of our own experiments on the effects of the full-size galanin and its chemically modified N-terminal fragments (2-11) and (2-15) on the heart in normal conditions and in modeling pathophysiological conditions in vitro and in vivo. It has been shown that the spectrum of the peptide actions on the damaged myocardium includes decrease in the necrotic death of cardiomyocytes, decrease in the damage of sarcolemma, improvement in the metabolic state of myocardium, decrease in the formation of reactive oxygen species (ROS) and lipid peroxidation (LPO) products. Mechanisms of the protective action of the modified galanin fragments associated with activation of the GalR2 receptor subtype and manifestation of antioxidant properties are discussed. The data summarized in the review indicate that the molecular design of pharmacological agonists of the GalR2 receptor is a promising approach, because they can serve as a basis for the development of cardioprotectors influencing processes of free radical oxidation and metabolic adaptation.

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KEY WORDS: galanin, heart, experimental pathology, reactive oxygen species, metabolism, cardiomyocyte membranes, lipid peroxidation, antioxidant enzymes

DOI: 10.1134/S000629792110014X

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