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OBJECTIVE: Atherosclerosis is characterized by chronic inflammation in the vascular wall. Currently the violation of immune tolerance of innate immune cells is considered as a possible mechanism of chronification of inflammation. The aim of this study is to assess the inflammatory activity and tolerance of monocytes and macrophages in subclinical atherosclerosis. METHODS: A total of 55 individuals free from clinical manifestations of atherosclerosis-associated cardiovascular disease with a presence or absence of atherosclerotic plaques in the carotid arteries were included in this study. CD14+ monocytes were isolated from individuals' blood and stimulated with a single dose of lipopolysaccharide (LPS) on day 1 or with double doses of LPS on day 1 and day 6. The secretion of cytokines TNF, IL-1ß, IL-6, IL-8, IL-10 and CCL2 were evaluated using ELISA. RESULTS: Our findings demonstrate that macrophages derived from LPS-stimulated monocytes in individuals with subclinical atherosclerosis exhibited increased secretion of IL-6, IL-10 and CCL2, which was associated with intima-media thickness, body mass index, but not with individuals' age. Moreover, macrophages from individuals with atherosclerotic plaques exhibited impaired tolerance towards the second LPS stimulation manifested by elevated secretion of the chemoattractant CCL2. CONCLUSION: Increased secretion of these cytokines by macrophages may contribute to chronic local inflammation in the vascular wall by recruiting other immune cells.
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Aterosclerose , Placa Aterosclerótica , Humanos , Monócitos , Lipopolissacarídeos/farmacologia , Interleucina-10 , Interleucina-6 , Espessura Intima-Media Carotídea , Macrófagos , Citocinas , InflamaçãoRESUMO
Osteoporosis is a widespread systemic disease characterized by a decrease in bone mass and an imbalance of the microarchitecture of bone tissue. Experimental and clinical studies devoted to investigating the main pathogenetic mechanisms of osteoporosis revealed the important role of estrogen deficiency, inflammation, oxidative stress, cellular senescence, and epigenetic factors in the development of bone resorption due to osteoclastogenesis, and decreased mineralization of bone tissue and bone formation due to reduced function of osteoblasts caused by apoptosis and age-depended differentiation of osteoblast precursors into adipocytes. The current review was conducted to describe the basic mechanisms of the development of osteoporosis at molecular and cellular levels and to elucidate the most promising therapeutic strategies of pathogenetic therapy of osteoporosis based on articles cited in PubMed up to September 2023.
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Osteogênese , Osteoporose , Humanos , Osteogênese/genética , Osteoblastos , Osteoporose/genética , Osteoporose/tratamento farmacológico , Osso e Ossos , Osteoclastos , Diferenciação CelularRESUMO
Cardiovascular diseases (CVD) and, in particular, atherosclerosis, remain the main cause of death in the world today. Unfortunately, in most cases, CVD therapy begins after the onset of clinical symptoms and is aimed at eliminating them. In this regard, early pathogenetic therapy for CVD remains an urgent problem in modern science and healthcare. Cell therapy, aimed at eliminating tissue damage underlying the pathogenesis of some pathologies, including CVD, by replacing it with various cells, is of the greatest interest. Currently, cell therapy is the most actively developed and potentially the most effective treatment strategy for CVD associated with atherosclerosis. However, this type of therapy has some limitations. In this review, we have tried to summarize the main targets of cell therapy for CVD and atherosclerosis in particular based on the analysis using the PubMed and Scopus databases up to May 2023.
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Aterosclerose , Doenças Cardiovasculares , Humanos , Doenças Cardiovasculares/etiologia , Aterosclerose/metabolismo , Terapia Baseada em Transplante de Células e Tecidos/efeitos adversos , Fatores de RiscoRESUMO
One of the problems of modern medical science is cardiovascular pathology caused by atherosclerotic vascular lesions in patients with autoimmune rheumatic diseases (ARDs). The similarity between the mechanisms of the immunopathogenesis of ARD and chronic low-grade inflammation in atherosclerosis draws attention. According to modern concepts, chronic inflammation associated with uncontrolled activation of both innate and acquired immunity plays a fundamental role in all stages of ARDs and atherosclerotic processes. Macrophage monocytes play an important role among the numerous immune cells and mediators involved in the immunopathogenesis of both ARDs and atherosclerosis. An imbalance between M1-like and M2-like macrophages is considered one of the causes of ARDs. The study of a key pathogenetic factor in the development of autoimmune and atherosclerotic inflammation-activated monocyte/macrophages will deepen the knowledge of chronic inflammation pathogenesis.
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Aterosclerose , Doenças Autoimunes , Placa Aterosclerótica , Síndrome do Desconforto Respiratório , Doenças Reumáticas , Aterosclerose/patologia , Humanos , Inflamação/patologia , Ativação de Macrófagos , Macrófagos , Placa Aterosclerótica/patologia , Doenças Reumáticas/patologiaRESUMO
Adipokines are currently widely studied cellular signaling proteins produced by adipose tissue and involved in various processes, including inflammation; energy and appetite modulation; lipid and glucose metabolism; insulin sensitivity; endothelial cell functioning; angiogenesis; the regulation of blood pressure; and hemostasis. The current review attempted to highlight the key functions of adipokines in the inflammatory mechanisms of obesity, its complications, and its associated diseases. An extensive search for materials on the role of adipokines in the pathogenesis of obesity was conducted online using the PubMed and Scopus databases until October 2022.
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Adipocinas , Resistência à Insulina , Humanos , Adipocinas/metabolismo , Obesidade/metabolismo , Tecido Adiposo/metabolismo , Inflamação/metabolismoRESUMO
Cardiovascular disease has been, and remains, one of the leading causes of death in the modern world. The elderly are a particularly vulnerable group. The aging of the body is inevitably accompanied by the aging of all its systems, and the cardiovascular system is no exception. The aging of the cardiovascular system is a significant risk factor for the development of various diseases and pathologies, from atherosclerosis to ischemic stroke. Mitochondria, being the main supplier of energy necessary for the normal functioning of cells, play an important role in the proper functioning of the cardiovascular system. The functioning of each individual cell and the organism as a whole depends on their number, structure, and performance, as well as the correct operation of the system in removing non-functional mitochondria. In this review, we examine the role of mitochondria in the aging of the cardiovascular system, as well as in diseases (for example, atherosclerosis and ischemic stroke). We pay special attention to changes in mitochondrial dynamics since the shift in the balance between fission and fusion is one of the main factors associated with various cardiovascular pathologies.
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Aterosclerose , Doenças Cardiovasculares , Sistema Cardiovascular , AVC Isquêmico , Idoso , Envelhecimento/patologia , Aterosclerose/patologia , Doenças Cardiovasculares/patologia , Sistema Cardiovascular/patologia , Humanos , Mitocôndrias/patologia , Dinâmica Mitocondrial/fisiologiaRESUMO
Cardiovascular diseases associated with atherosclerosis are the major cause of death in developed countries. Early prevention and treatment of atherosclerosis are considered to be an important aspect of the therapy of cardiovascular disease. Preparations based on natural products affect the main pathogenetic steps of atherogenesis, and so represent a perspective for the long-term prevention of atherosclerosis development. Numerous experimental and clinical studies have demonstrated the multiple beneficial effects of licorice and its bioactive compounds-anti-inflammatory, anti-cytokine, antioxidant, anti-atherogenic, and anti-platelet action-which allow us to consider licorice as a promising atheroprotective agent. In this review, we summarized the current knowledge on the licorice anti-atherosclerotic mechanisms of action based on the results of experimental studies, including the results of the in vitro study demonstrating licorice effect on the ability of blood serum to reduce intracellular cholesterol accumulation in cultured macrophages, and presented the results of clinical studies confirming the ameliorating activity of licorice in regard to traditional cardiovascular risk factors as well as the direct anti-atherosclerotic effect of licorice.
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Aterosclerose , Glycyrrhiza , Anti-Inflamatórios/farmacologia , Anti-Inflamatórios/uso terapêutico , Antioxidantes/farmacologia , Aterosclerose/tratamento farmacológico , Aterosclerose/prevenção & controle , Humanos , Extratos Vegetais/farmacologia , Extratos Vegetais/uso terapêuticoRESUMO
Chronic stress is a combination of nonspecific adaptive reactions of the body to the influence of various adverse stress factors which disrupt its homeostasis, and it is also a corresponding state of the organism's nervous system (or the body in general). We hypothesized that chronic stress may be one of the causes occurence of several molecular and cellular types of stress. We analyzed literary sources and considered most of these types of stress in our review article. We examined genes and mutations of nuclear and mitochondrial genomes and also molecular variants which lead to various types of stress. The end result of chronic stress can be metabolic disturbance in humans and animals, leading to accumulation of reactive oxygen species (ROS), oxidative stress, energy deficiency in cells (due to a decrease in ATP synthesis) and mitochondrial dysfunction. These changes can last for the lifetime and lead to severe pathologies, including neurodegenerative diseases and atherosclerosis. The analysis of literature allowed us to conclude that under the influence of chronic stress, metabolism in the human body can be disrupted, mutations of the mitochondrial and nuclear genome and dysfunction of cells and their compartments can occur. As a result of these processes, oxidative, genotoxic, and cellular stress can occur. Therefore, chronic stress can be one of the causes forthe occurrence and development of neurodegenerative diseases and atherosclerosis. In particular, chronic stress can play a large role in the occurrence and development of oxidative, genotoxic, and cellular types of stress.
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Aterosclerose/metabolismo , Aterosclerose/patologia , Doenças Neurodegenerativas/metabolismo , Doenças Neurodegenerativas/patologia , Estresse Oxidativo/fisiologia , Animais , Homeostase/fisiologia , Humanos , Mitocôndrias/metabolismo , Mitocôndrias/patologia , Espécies Reativas de Oxigênio/metabolismoRESUMO
Myocardial edema is the excess accumulation of fluid in the myocardial interstitium or cardiac cells that develops due to changes in capillary permeability, loss of glycocalyx charge, imbalance in lymphatic drainage, or a combination of these factors. Today it is believed that this condition is not only a complication of cardiovascular diseases, but in itself causes aggravation of the disease and increases the risks of adverse outcomes. The study of molecular, genetic, and mechanical changes in the myocardium during edema may contribute to the development of new approaches to the diagnosis and treatment of this condition. This review was conducted to describe the main mechanisms of myocardial edema development at the molecular and cellular levels and to identify promising targets for the regulation of this condition based on articles cited in Pubmed up to January 2024.
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BACKGROUND: Metabolic disorders, including obesity, are often accompanied by an increased risk of cardiovascular complications. Monocytes are the common link between obesity and cardiovascular diseases (CVDs). The bias of innate cellular immunity towards pro-inflammatory activation stimulates the development of diseases associated with chronic inflammation, in particular metabolic disorders, including obesity, as well as CVDs. Disorders in the functional state of monocytes and activation of inflammation may be associated with mitochondrial dysfunction. Mutations accumulating in mitochondrial DNA with age may lead to mitochondrial dysfunction and may be considered a potential marker for developing chronic inflammatory diseases. METHODS: The present study aimed to study the relationship between mitochondrial heteroplasmy in CD14+ monocytes and cardiovascular risk factors in 22 patients with obesity and coronary heart disease (CHD) by comparing them to 22 healthy subjects. RESULTS: It was found that single-nucleotide variations (SNV) A11467G have a negative correlation with total cholesterol (r = -0.82, p < 0.05), low density lipoproteins (LDL) (r = -0.82, p < 0.05), with age (r = -0.57, p < 0.05) and with mean carotid intima-media thickness (cIMT) (r = -0.43, p < 0.05) and a positive correlation with HDL level (r = 0.71, p < 0.05). SNV 576insC positively correlated with body mass index (BMI) (r = 0.60, p < 0.001) and LDL level (r = 0.43, p < 0.05). SNV A1811G positively correlated with mean cIMT (r = 0.60, p < 0.05). CONCLUSIONS: It was revealed that some variants of mitochondrial DNA (mtDNA) heteroplasmy are associated with CVD risk factors. The results demonstrate the potential for using these molecular genetic markers to develop personalized CVD and metabolic disorder treatments.
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Doenças Cardiovasculares , Doença das Coronárias , Genoma Mitocondrial , Doenças Metabólicas , Doenças Mitocondriais , Humanos , Espessura Intima-Media Carotídea , Monócitos , Genoma Mitocondrial/genética , Doença das Coronárias/genética , Obesidade/complicações , Obesidade/genética , Fatores de Risco , Inflamação , Biomarcadores , Mutação/genética , DNA Mitocondrial/genéticaRESUMO
BACKGROUND: Investigation of the inflammatory response of immune cells is a current focus of research on autoimmune disorders. The aim of this study was to evaluate the inflammatory status of monocytes/macrophages in systemic sclerosis (SSc). METHODS: The study included 35 SSc and 25 healthy participants. The secretion of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8), interleukin-6 (IL-6) was measured by enzyme-linked immunosorbent assay (ELISA) in primary cultures of monocytes/macrophages after stimulation with lipopolysaccharide (LPS) on day 1 and on day 6 of incubation. Impaired tolerance of the immune response was characterized by increased secretion of the inflammatory mediators in response to restimulation. RESULTS: Basal secretion of all cytokines was significantly higher in SSc patients compared to healthy individuals. The secretion of TNF-α, IL-1ß and IL-6 after the initial LPS stimulation, and secretion of IL-1ß, MCP-1, IL-6, IL-8 after LPS restimulation, was significantly higher in the SSc group. Eleven SSc patients (31%) showed impaired immune tolerance in terms of MCP-1 secretion. These patients were significantly younger and had a higher level of anti-topoisomerase I (anti-Scl70) antibodies compared to SSc patients with immune tolerance. CONCLUSIONS: This study revealed pro-inflammatory activation and impaired immune tolerance in monocytes/macrophages from SSc patients. The violation of immune response in terms of MCP-1 secretion may be an important factor in the development of chronic inflammation in SSc. MCP-1 may thus be a potential therapeutic target for novel SSc treatment strategies.
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Macrófagos , Monócitos , Escleroderma Sistêmico , Humanos , Escleroderma Sistêmico/imunologia , Escleroderma Sistêmico/metabolismo , Monócitos/imunologia , Monócitos/metabolismo , Feminino , Masculino , Pessoa de Meia-Idade , Macrófagos/imunologia , Macrófagos/metabolismo , Adulto , Inflamação/imunologia , Lipopolissacarídeos , Citocinas/metabolismo , Citocinas/imunologia , Estudos de Casos e Controles , Quimiocina CCL2/metabolismo , Quimiocina CCL2/imunologia , Idoso , Ensaio de Imunoadsorção Enzimática , Interleucina-1beta/metabolismo , Interleucina-1beta/imunologiaRESUMO
Introduction: Mitochondrial dysfunction may be one of the causes of inflammatory activation of monocytes and macrophages, which leads to excessive secretion of inflammatory mediators and the development of chronic inflammation. Aims: The study was aimed to evaluate the secretion of inflammatory cytokine tumor necrosis factor-α (TNF-α) in the primary culture of monocytes, and to analyze its relationship with the number of mitochondrial DNA (mtDNA) copies in the blood of patients with coronary heart disease (CHD) and obesity. Materials and methods: 108 patients with obesity and concomitant CHD and a control group of 25 participants were included in the study. CD14+ monocytes were isolated by a standard method in a ficoll-urographin gradient, followed by separation using magnetic particles. The number of mtDNA copies was estimated using qPCR. Results: It was demonstrated that the number of mtDNA copies was significantly increased in groups of patients with CHD and obesity + CHD in comparison with control group. mtDNA copy number positively correlated with basal and LPS-stimulated TNF-α secretion, the most significant correlation was found in the group of patients with CHD and obesity. Conclusion: Thus, the change in mtDNA copy number in CD14+ monocytes which indicates the presence of mitochondrial dysfunction, confirm the direct involvement of mitochondria in the violation of the inflammatory response of monocytes revealed in this study as an increased secretion of inflammatory cytokine TNF-α.
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OBJECTIVE: To evaluate the rate of subclinical carotid atherosclerosis and clinical significance of immunoinflammatory markers in patients with rheumatoid arthritis (RA) at low cardiovascular risk. MATERIALS AND METHODS: The study included 275 RA patients and a control group of 100 participants without autoimmune diseases. All study participants were at low cardiovascular risk, calculated by the QRISK3 scale (<20%), and free of cardiovascular disease. Ultrasound examination of carotid arteries was performed to measure cIMT and to detect atherosclerotic plaques (ASP) in carotid arteries. sIСÐÐ-1, sVСÐÐ, and sCD40L levels were determined by enzyme immunoassay. RESULTS: Carotid ASP was observed more frequently in RA patients (27%) than in the control group (17%), p = 0.03. The frequency of ASP in RA patients did not depend on the disease's stage or activity. There was a significant correlation between cIMT and age, cardiovascular risk determined by QRISK3, level of total cholesterol, LDL, and blood pressure in RA patients, p < 0.05 in all cases. No correlation between cIMT and blood levels of sCD40L, sVCAM, and sICAM was found. In RA patients, a higher concentration of sVCAM was detected in the carotid ASP group compared to the non-atherosclerotic group. sCD40L was associated with cIMT and total cholesterol in the ASP group and with total cholesterol and blood pressure in non-atherosclerotic patients. CONCLUSIONS: Subclinical atherosclerotic lesions of the carotid arteries were observed significantly more frequently in RA patients with low cardiovascular risk than in the control group. The results of the study demonstrate the association between cIMT, traditional cardiovascular risk factors, and immunoinflammatory markers in RA patients.
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Exosomes are natural extracellular vesicles that play a key role in inter- and intracellular communication. Currently they are considered as a promising therapeutic strategy for the treatment of various diseases. In osteoimmunology, exosomes can serve as biomarkers of bone homeostasis disorders and, at the same time, promising therapeutic agents with high stability in the biological environment, low immunogenicity and good bioavailability. In this review, we attempted to examine exosomes as natural mediators of intercellular communication, playing an essential role in the interaction of the immune system and bone tissue, based on an analysis of the PubMed database up to October 2023.
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Exossomos , Vesículas Extracelulares , Comunicação Celular , Biomarcadores , Sistema ImunitárioRESUMO
BACKGROUND: Mitochondrial dysfunction is considered an important mechanism in the pathogenesis of various diseases. Therefore, mitochondria are currently being considered as subjects for targeted therapies, particularly, phototherapy using 5-aminolevulinic acid. This study aimed to investigate the activity of mitochondria in cells with different mutation loads. MATERIALS AND METHODS: The study was conducted using 11 cybrid lines obtained from the THP-1 cell line (a human monocytic leukemia cell line) and platelets of patients with different mitochondrial mutations. RESULTS: Our results illustrate that 5-aminolevulinic acid was metabolized equally in all cell lines, however, there was a significant decrease in mitochondrial potential, which differed among lines. CONCLUSIONS: The results of this study can be used to develop a personalized therapeutic approach based on different mitochondrial activities.
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Ácido Aminolevulínico , Fármacos Fotossensibilizantes , Humanos , Ácido Aminolevulínico/farmacologia , Ácido Aminolevulínico/metabolismo , Fármacos Fotossensibilizantes/farmacologia , Fármacos Fotossensibilizantes/metabolismo , Fármacos Fotossensibilizantes/uso terapêutico , Mitocôndrias/metabolismo , Linhagem Celular , Células THP-1 , Linhagem Celular TumoralRESUMO
Introduction: Systemic scleroderma (SSc) is a chronic autoimmune disease of inflammatory origin. Mitochondrial dysfunction is considered as an important mechanism in the pathogenesis of SSc. Currently mitochondrial DNA (mtDNA) copy number is used as a surrogate marker of mitochondrial dysfunction. Previous studies demonstrate that innate immune cells are important participants in inflammatory and fibrotic processes in SSc. The aim of the study was to evaluate the number of mtDNA copies in CD14+ monocytes and whole blood of patients with SSc in comparison with healthy individuals. Methods: Absolute mtDNA copy number was measured using digital PCR. It was found that the number of mtDNA copies in CD14+ monocytes was significantly higher in patients with SSc compared to control, while the number of mtDNA copies in the whole blood did not have significant differences. Results: The correlation analysis revealed an inverse association of mtDNA copy number with disease duration and the relationship between pro-inflammatory activation of CD14+ monocytes in terms of LPS-stimulated IL-6 secretion and mtDNA copy number. At the same time, basal and LPS-stimulated secretion of IL-6 by cultured CD+ monocytes were significantly higher in SSc group in comparison with control. Discussion: The study results suggest that increase of mtDNA copy number in CD14+ monocytes is a possible mechanism to maintain the reduced function of defective mitochondria in monocytes from patients with SSc associated with the development and progression of SSc.
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The great importance of diet for health and high life-expectancy is established. The impact of nutrients on immune system is a point of growing research interest. Recent studies have found pro- and anti-inflammatory properties of some diet patterns and nutrients that can be used from the bench to the bedside for chronic low-grade inflammatory status correction. In this regard, the assessment of potential effects of nutrition on macrophage differentiation, proliferation, and functioning in health and disease is highly demanded. In this review, we present current data on the effects of nutrients on the macrophage functioning.
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The main cause of death in patients with type 2 DM is cardiovascular complications resulting from the progression of atherosclerosis. The pathophysiology of the association between diabetes and its vascular complications is complex and multifactorial and closely related to the toxic effects of hyperglycemia that causes increased generation of reactive oxygen species and promotes the secretion of pro-inflammatory cytokines. Subsequent oxidative stress and inflammation are major factors of the progression of type 2 DM and its vascular complications. Data on the pathogenesis of the development of type 2 DM and associated cardiovascular diseases, in particular atherosclerosis, open up broad prospects for the further development of new diagnostic and therapeutic approaches.
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Recent studies have shown that cellular metabolism is tightly linked to the regulation of immune cells. Here, we show that activation of cholesterol metabolism, involving cholesterol uptake, synthesis, and autophagy/lipophagy, is integral to innate immune responses in macrophages. In particular, cholesterol accumulation within endosomes and lysosomes is a hallmark of the cellular cholesterol dynamics elicited by Toll-like receptor 4 activation and is required for amplification of myeloid differentiation primary response 88 (Myd88) signaling. Mechanistically, Myd88 binds cholesterol via its CLR recognition/interaction amino acid consensus domain, which promotes the protein's self-oligomerization. Moreover, a novel supramolecular compound, polyrotaxane (PRX), inhibited Myd88dependent inflammatory macrophage activation by decreasing endolysosomal cholesterol via promotion of cholesterol trafficking and efflux. PRX activated liver X receptor, which led to upregulation of ATP binding cassette transporter A1, thereby promoting cholesterol efflux. PRX also inhibited atherogenesis in Ldlr-/- mice. In humans, cholesterol levels in circulating monocytes correlated positively with the severity of atherosclerosis. These findings demonstrate that dynamic changes in cholesterol metabolism are mechanistically linked to Myd88dependent inflammatory programs in macrophages and support the notion that cellular cholesterol metabolism is integral to innate activation of macrophages and is a potential therapeutic and diagnostic target for inflammatory diseases.
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Aterosclerose , Macrófagos , Camundongos , Humanos , Animais , Membro 1 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/metabolismo , Macrófagos/metabolismo , Aterosclerose/metabolismo , Colesterol/metabolismo , Receptores X do Fígado/metabolismo , Fator 88 de Diferenciação Mieloide/metabolismoRESUMO
Background: Coronavirus disease 2019 (COVID-19) might affect everyone, but people with comorbidities such as hypertension and cardiovascular disease (CVD) may often have more severe complications and worse outcomes. Although vaccinations are being performed worldwide, it will take a long time until the entire population of the world is vaccinated. On the other hand, we are witnessing the emergence of new variants of this virus. Therefore, effective therapeutic approaches still need to be considered. Statins are well-known lipid-lowering drugs, but they have also anti-inflammatory and immunomodulatory effects. This study aimed to investigate the effects of statins on the survival of COVID-19 hospitalized patients. Methods: This retrospective study was performed on 583 patients admitted to a highly referenced hospital in Tabas, Iran, between February 2020 and December 2020. One hundred sixty-two patients were treated with statins and 421 patients were not. Demographic information, clinical signs, and the results of laboratory, and comorbidities were extracted from patients' medical records and mortality and survival rates were assessed in these two groups. Results: The results of the Cox crude regression model showed that statins reduced mortality in COVID-19 patients (HR = 0.56, 95% CI: 0.32, 0.97; p = 0.040), although this reduction was not significant in the adjusted model (HRs=0.51, 95%CI: 0.22, 1.17; p = 0.114). Using a composite outcome comprising intubation, ICU admission, and mortality, both crude (HR = 0.43; 95% CI: 0.26, 0.73; p = 0.002) and adjusted (HR = 0.57; 95% CI: 0.33, 0.99; p = 0.048) models suggested a significant protective effect of statin therapy. Conclusion: Due to anti-inflammatory properties of statins, these drugs can be effective as an adjunct therapy in the treatment of COVID-19 patients.