Cardiovascular, rheumatic, kidney, and neurodegenerative diseases and mental disorders are a common cause of deterioration in the quality of life up to severe disability and death worldwide. Many pathological conditions, including this group of diseases, are based on increased cell death through apoptosis. It is known that this process is associated with signaling pathways controlled by a group of gaseous signaling molecules called gasotransmitters. They are unique messengers that can control the process of apoptosis at different stages of its implementation. However, their role in the regulation of apoptotic signaling in these pathological conditions is often controversial and not completely clear. This review analyzes the role of nitric oxide (NO), carbon monoxide (CO), hydrogen sulfide (H2S), and sulfur dioxide (SO2) in apoptotic cell death in cardiovascular, rheumatic, kidney, and neurodegenerative diseases. The signaling processes involved in apoptosis in schizophrenia, bipolar, depressive, and anxiety disorders are also considered. The role of gasotransmitters in apoptosis in these diseases is largely determined by cell specificity and concentration. NO has the greatest dualism; scales are more prone to apoptosis. At the same time, CO, H2S, and SO2 are more involved in cytoprotective processes.

Injuries of the central (CNS) and peripheral nervous system (PNS) are a serious problem of the modern healthcare system. The situation is complicated by the lack of clinically effective neuroprotective drugs that can protect damaged neurons and glial cells from death. In addition, people who have undergone neurotrauma often develop mental disorders and neurodegenerative diseases that worsen the quality of life up to severe disability and death. Hydrogen sulfide (H2S) is a gaseous signaling molecule that performs various cellular functions in normal and pathological conditions. However, the role of H2S in neurotrauma and mental disorders remains unexplored and sometimes controversial. In this large-scale review study, we examined the various biological effects of H2S associated with survival and cell death in trauma to the brain, spinal cord, and PNS, and the signaling mechanisms underlying the pathogenesis of mental illnesses, such as cognitive impairment, encephalopathy, depression and anxiety disorders, epilepsy and chronic pain. We also studied the role of H2S in the pathogenesis of neurodegenerative diseases: Alzheimer’s disease (AD) and Parkinson’s disease (PD). In addition, we reviewed the current state of the art study of H2S donors as neuroprotectors and the possibility of their therapeutic uses in medicine. Our study showed that H2S has great neuroprotective potential. H2S reduces oxidative stress, lipid peroxidation, and neuroinflammation; inhibits processes associated with apoptosis, autophagy, ferroptosis and pyroptosis; prevents the destruction of the blood-brain barrier; increases the expression of neurotrophic factors; and models the activity of Ca2+ channels in neurotrauma. In addition, H2S activates neuroprotective signaling pathways in psychiatric and neurodegenerative diseases. However, high levels of H2S can cause cytotoxic effects. Thus, the development of H2S-associated neuroprotectors seems to be especially relevant. However, so far, all H2S modulators are at the stage of preclinical trials. Nevertheless, many of them show a high neuroprotective effect in various animal models of neurotrauma and related disorders. Despite the fact that our review is very extensive and detailed, it is well structured right down to the conclusions, which will allow researchers to quickly find the proper information they are interested in.

Ростовский государственный медицинский университет, Ростов-на-Дону, Россия chronic ischemic disease of The digesTiVe sYsTem: diagnosTic proBlems and iTs soluTions Bogatirev V. g., marinchuk a. T., gasanov m. Z., Terentyev V. p., Tkachev a. V. rostov state medical university, rostov-on-don, russia Хроническая ишемическая болезнь органов пищеварения (ХИБОП)-редкое заболевание, которое проявляется появлением абдоминальных болей после еды и потерей массы тела. Ввиду неспецифичности жалоб, отсутствия патогномоничных признаков при объективном обследовании, недостаточной настороженности врачей верификация болезни представляется сложной, и зачастую ХИБОП является диагнозом исключения. Вместе с тем оценка факторов риска (возраст пациента, высокая степень коморбидности, факторы риска атеросклероза, наличие васкулопатий в бассейнах нескольких артерий и др.) наряду с инструментальным обследованием, включающим триплексное УЗИ, ангиографию, МРТ, КТ-ангиографию, тонометрию, может существенно повысить выявление ХИБОП. Представлен актуальный взгляд на проблему с обзором современной литературы, а также клинический разбор пациента с хронической абдоминальной ишемией, длительно наблюдавшегося по поводу патологии желудочно-кишечного тракта неишемического генеза. Ключевые слова: хроническая ишемическая болезнь органов пищеварения, стентирование, окклюзия верхней брыжеечной артерии Chronic ischemic disease of the digestive system (СIDDS) is a rare pathology which is manifested by the abdominal pain after meals and weight loss. In view of the non-specific nature of complaints, the absence of pathognomonic signs in an objective examination, the lack of alertness of doctors, the verification is complex, and often СIDDS is the diagnosis of exclusion. However, an assessment of the risk factors (patient age, high degree of comorbidity, atherosclerosis risk factors, the presence of vasculopathies in several arterial basins) along with the proper instrumental examination, including triplex ultrasound, angiography, MRI, CT angiography, tonometry can significantly improve the identification of СIDDS. This article presents a modern approach to the problem of СIDDS with the review of the current literature, as well as a clinical case of the patient with chronic abdominal ischemia, which has been observed for a long time for the gastrointestinal tract pathology of non-ischemic origin.

Исследования, выполненные в его лабораториях и посвященные поискам взаимосвязи между холестерином жирной пищи и эксперимен-тальным атеросклерозом сделали Александра Иосифовича одним из основоположников учения об атеросклерозе в мире. Это достижение было признано в США одним из 10 важнейших открытий в медицине и описано в книге с одноименным названием. Его новаторские работы заложили прочную основу для дальнейших исследований в области липидологии. В Германии проф. К.Т. Фар, в России -Аничков Н.Н.и Халатов С.С. были одними из первых, кто использовали экспериментальные протоколы Игнатовского и успешно воспроизвели его опыты.Благодаря этой обширной работе, сегодня мы имеем детальные представления о патофизиологии атеросклероза, о причинах его возник-новения, последствиях его развития, методах диагностики и лечения, а также можем рассчитывать риск сердечно-сосудистых событий и влиять на продолжительность жизни. Богатое научное наследие, оставленное им, до сих пор не утратило своей актуальности, а гипотезы, выдвинутые им почти сто лет назад, многократно подтвердились. were among the first scientists who used the experimental protocols of Ignatowski and successfully reproduced his experiments. Thanks to this extensive work, today we have detailed knowledge of the pathophysiology of atherosclerosis, the causes of its occurrence, the consequences of its development, the methods of diagnosis and treatment, and can calculate the risk of cardiovascular events and influence life expectancy. Ключевые слова: профессор Игнатовский Александр Иосифович, атеросклероз, Императорский Варшавский университет

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