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Editor's Letter
Journal: Non Nocere. New Therapeutic Journal. 2025;(9): 1‑1
Read: 251 times
To cite this article:
We've decided to dedicate this issue to cardiology. We'll cover complex patients, algorithms for practicing physicians, and a discussion of cardiopathy. But the theme of atherosclerosis will be a common thread throughout the journal. Let's look back. The story begins in ancient Egypt: the Ebers Papyrus describes "petrified vessels," likely the first observations of calcified aortas. More than three thousand years have passed since then, but interest in the nature of vascular aging hasn't waned for a day.
In the 19th century, Rudolf Virchow viewed atherosclerosis as an inflammatory process, while Karl Rokitansky believed it was the result of thrombus formation. Their debate became the starting point for the scientific understanding of the disease. At the beginning of the 20th century, Nikolai Anichkov, conducting his classic experiments with cholesterol in rabbits, demonstrated its crucial role in plaque formation—albeit primitively, but insightfully. Fredrickson subsequently proposed a classification of hyperlipoproteinemias, and the work of Michael Brown and Joseph Goldstein uncovered the role of LDL receptors, demonstrating the genetic nature of some forms of hypercholesterolemia.
From this point on, atherosclerosis began to be viewed as a multifactorial, systemic process, intertwining not only metabolism and heredity. The modern concept sees atherosclerosis as chronic inflammation of the vascular wall, of which lipid abnormalities are only one facet. Therapy is now aimed not only at lowering cholesterol levels, but also at key elements of the inflammatory and genetic cascade – from cytokines to inflammasomes.
From the "stone aortas" of the ancient Egyptians to the molecular interventions of the 21st century – this is a history of exploration, doubt, and discovery, bringing us closer to understanding how blood vessels function and age.
Enjoy reading!
Professor I.V. Egorov
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