Aortic Aneurysm with and without Dissection and Concomitant Atherosclerosis-Differences in a Retrospective Study.

Background: Thoracic aortic aneurysm is a latent disease with a high risk of death. Today, as data are accumulating, an estimation of the differences in thoracic aneurysm in men and women of different age groups is required. The present study evaluated the type of atherosclerotic aortic lesions in males and females at different ages regarding the presence or absence of aortic dissection.

Analysis of Mutational Burden of Mitochondrial Genome in Cells of Different Human Organs and Tissues.

Background: Cells of different human organs and tissues contain different numbers of mitochondria. In these organelles, there are different copies of the mitochondrial genome, which is characteristic of a certain organ or tissue.

Objective: The aim of the investigation was to analyze the results of scientific works dedicated to the analysis of heteroplasmy levels of mitochondrial genome mutations in a number of organs and tissues.

Target Role of Monocytes as Key Cells of Innate Immunity in Rheumatoid Arthritis.

Rheumatoid arthritis (RA) is a chronic, systemic, and inflammatory autoimmune condition characterized by synovitis, pannus formation (with adjacent bone erosion), and joint destruction. In the perpetuation of RA, fibroblast-like synoviocytes (FLSs), macrophages, B cells, and CD4 T-cells-specifically Th1 and Th17 cells-play crucial roles. Additionally, dendritic cells, neutrophils, mast cells, and monocytes contribute to the disease progression.

The role of mitochondria in metastasis development.

Metastasis is a hallmark of cancer and is responsible for the largest number of cancer-related deaths. However, it remains poorly understood. Recently, evidence has accumulated pointing to the role of mitochondria in the metastatic spread of cancer cells.

Significance of Mitochondrial Dysfunction in the Pathogenesis of Parkinson's Disease.

Parkinson's disease (PD) is characterized by the degeneration of the dopaminergic neurons of the corpus striatum, which can be caused by the disruption of processes of mitochondrial homeostasis, including mitophagy, mitochondrial fusion and division, mitochondrial transport, accumulation of reactive oxygen species (ROS), and calcium signaling. Dopaminergic neurons are particularly vulnerable to mitochondrial dysfunction due to their polarized and expanded structure and high bioenergy needs. The molecular basis of these disorders is manifested in mutations of mitochondrial homeostasis proteins.

Molecular and Cellular Mechanisms of Osteoporosis.

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.

The Role of Mitochondrial Dysfunction in the Development of Acute and Chronic Hepatitis С.

Currently, the issue relating to the discussion raised in this article appears to be for what purposes the hepatitis C virus (HCV) modulates cellular processes, such as antiviral defense, metabolism, apoptosis, and mitochondrial dynamics, by inhibiting the activity or expression of mitochondrial proteins and a number of cellular proteins. Additionally, to what pathological changes do these alterations lead? Thus, the aim of this review is to propose potential protein mitochondrial targets of HCV for the future development of new drugs aimed at inhibiting its interaction with cellular proteins. Considering current analyses in the literature, promising targets for the acute and chronic phases of HCV are proposed which include mitochondrial antiviral signaling (MAVS) (antiviral response protein), Parkin (mitophagy protein), Drp1 (mitochondrial fission protein), subunits 1 and 4 of the electron transport chain (ETC) complex (oxidative phosphorylation proteins), among others.

Mechanisms of the Wnt Pathways as a Potential Target Pathway in Atherosclerosis.

The proteins of the Wnt family are involved in a variety of physiological processes by means of several canonical and noncanonical signaling pathways. Wnt signaling has been recently identified as a major player in atherogenesis. In this review, we summarize the existing knowledge on the influence of various components of the Wnt signaling pathways on the initiation and progression of atherosclerosis and associated conditions.

Is There a Relationship between Adverse Pregnancy Outcomes and Future Development of Atherosclerosis?

Cardiovascular disease is one of the main death causes globally. Effective cardiovascular risk management requires a thorough understanding of the mechanisms underlying the disorder. Establishing early markers of the disease allows a timely intervention and prevention of further atherosclerosis development.

Tumor Suppressor Properties of Small C-Terminal Domain Phosphatases in Clear Cell Renal Cell Carcinoma.

Clear cell renal cell carcinoma (ccRCC) accounts for 80-90% of kidney cancers worldwide. Small C-terminal domain phosphatases CTDSP1, CTDSP2, and CTDSPL (also known as SCP1, 2, 3) are involved in the regulation of several important pathways associated with carcinogenesis. In various cancer types, these phosphatases may demonstrate either antitumor or oncogenic activity.

Sex Differences Define the Vulnerability to Atherosclerosis.

For several decades, atherosclerosis has attracted the attention of researchers around the world. Even being a major cause of serious cardiovascular disease and events, atherosclerosis is still not fully understood. Despite the fact that the main players in the pathogenesis of atherosclerosis are well known, many mechanisms of their implementation and interactions remain unknown.

Target and Cell Therapy for Atherosclerosis and CVD.

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.

Condition "Vasa Vasorum" in Patients with Thoracic Aortic Aneurysm.

It is known that vasa vasorum contributes substantially to the blood supply and nutrition of one-third of the wall of the ascending thoracic aorta. Therefore, we focused on studying the relationship between inflammatory cells and vasa vasorum vessels in patients with aortic aneurysm. The material for the study was biopsies of thoracic aortic aneurysms taken from patients during an aneurysmectomy (34 men, 14 women, aged 33 to 79 years).

The Neuroimmune Role of Intestinal Microbiota in the Pathogenesis of Cardiovascular Disease.

Currently, a bidirectional relationship between the gut microbiota and the nervous system, which is considered as microbiota-gut-brain axis, is being actively studied. This axis is believed to be a key mechanism in the formation of somatovisceral functions in the human body. The gut microbiota determines the level of activation of the hypothalamic-pituitary system.

An original biomarker for the risk of developing cardiovascular diseases and their complications: Telomere length.

Aim: The aim of this work was to study the effect of telomere length in the chromosomes of nuclear blood cells in individuals with coronary heart disease (CHD) on the development of cardiovascular complications (CVC).

Materials And Methods: DNA was isolated from nuclear blood cells of 498 study participants. The telomere length was determined by real-time polymerase chain reaction.

Thoracic Aortic Aneurysm: Blood Pressure and Inflammation as Key Factors in the Development of Aneurysm Dissection.

Aortic aneurism development is dependent on internal and external etiological factors that define the width of the therapeutic window available for the treatment of patients with such diagnosis. In this review, we provide a detailed overview of the most prominent of these factors. In particular, we discuss the input of elevated blood pressure to the remodeling of the aortic wall, describe the mechanisms of inflammatory remodeling of the aorta, and evaluate the cross-interaction of blood pressure, inflammation and immunity during the pathology development.

Thoracic Aortic Aneurysm and Factors Affecting Aortic Dissection.

This study is aimed at investigating the relationship between inflammation, the number of vasa vasorum, and the presence of lipoprotein (a) [Lp(a)] in the aortic aneurysm wall, as well as the relationships of these pathological processes with the development of aneurysm wall dissection. To that end, we examined segments of aortic aneurysm wall, consisting of intima, media, and adventitia, collected from patients during aneurysm prosthetics intervention. The material was collected from 23 men and eight women aged from 33 to 69 years.

Heteroplasmic Variants of Mitochondrial DNA in Atherosclerotic Lesions of Human Aortic Intima.

Mitochondrial dysfunction and oxidative stress are likely involved in atherogenesis. Since the mitochondrial genome variation can alter functional activity of cells, it is necessary to assess the presence in atherosclerotic lesions of mitochondrial DNA (mtDNA) heteroplasmic mutations known to be associated with different pathological processes and ageing. In this study, mtDNA heteroplasmy and copy number (mtCN) were evaluated in the autopsy-derived samples of aortic intima differing by the type of atherosclerotic lesions.

Mitochondrial diseases caused by mtDNA mutations: a mini-review.

There are several types of mitochondrial cytopathies, which cause a set of disorders, arise as a result of mitochondria's failure. Mitochondria's functional disruption leads to development of physical, growing and cognitive disabilities and includes multiple organ pathologies, essentially disturbing the nervous and muscular systems. The origins of mitochondrial cytopathies are mutations in genes of nuclear DNA encoding mitochondrial proteins or in mitochondrial DNA.

Cybrid Models of Pathological Cell Processes in Different Diseases.

Modelling of pathological processes in cells is one of the most sought-after technologies of the 21st century. Using models of such processes may help to study the pathogenetic mechanisms of various diseases. The aim of the present study was to analyse the literature, dedicated to obtaining and investigating cybrid models.

Role of Mitochondrial Genome Mutations in Pathogenesis of Carotid Atherosclerosis.

Mutations of mtDNA, due to their higher frequency of occurrence compared to nuclear DNA mutations, are the most promising biomarkers for assessing predisposition of the occurrence and development of atherogenesis. The aim of the present article was an analysis of correlation of several mitochondrial genome mutations with carotid atherosclerosis. Leukocytes from blood of study participants from Moscow polyclinics were used as research material.