Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Background: The present review article considers some chronic diseases of vascular and metabolic genesis, the causes of which may be mitochondrial dysfunction. Very often, in the long course of the disease, complications may occur, leading to myocardial infarction or ischemic stroke and, as a result, death. In particular, a large percentage of human deaths nowadays belongs to cardiovascular diseases, such as coronary heart disease (CHD), arterial hypertension, cardiomyopathies, and type 2 diabetes mellitus.

Objective: The aim of the present review was the analysis of literature sources, devoted to an investigation of a link of mitochondrial DNA mutations with chronic diseases of vascular and metabolic genesis.

Results: The analysis of literature indicates the association of the mitochondrial genome mutations with coronary heart disease, type 2 diabetes mellitus, hypertension, and various types of cardiomyopathies.

Conclusion: The detected mutations can be used to analyze the predisposition to chronic diseases of vascular and metabolic genesis. They can also be used to create molecular-cell models necessary to evaluate the effectiveness of drugs developed for the treatment of these pathologies. MtDNA mutations associated with the absence of diseases of vascular and metabolic genesis could be potential candidates for gene therapy of the said diseases.

Download full-text PDF

Source
http://dx.doi.org/10.2174/1381612826999200820162154DOI Listing

Publication Analysis

Top Keywords

vascular metabolic
20
diseases vascular
16
chronic diseases
12
metabolic genesis
12
coronary heart
8
heart disease
8
type diabetes
8
analysis literature
8
diseases
7
mutations
5

Similar Publications

Objective: Aim: To evaluate the state of oxidation processes and morphological changes in the heart of rats with chronic hypodynamia during the development of epinephrine heart damage (EHD)..

Patients And Methods: Materials and Methods: The study was performed on 144 white male Wistar rats.

View Article and Find Full Text PDF

Purpose: We aimed to compare the effects of atelocollagen (AC) and individual growth factors on the expression of key molecular markers associated with tendon healing.

Methods: C2C12 myoblasts were cultured in Dulbecco's Modified Eagle Medium (DMEM) containing 5% fetal bovine serum (FBS) and treated with 1 nM or 10 nM of Atelocollagen (AC), bone morphogenetic protein-2 (BMP-2), transforming growth factor-beta 1 (TGF-β1), insulin-like growth factor-1 (IGF-1), or vascular endothelial growth factor (VEGF) for 5 days. After 5 days of treatment, cells were harvested from the culture medium, and Western blot analysis was performed to quantify the expression of phosphorylated extracellular signal-regulated kinase (p-ERK), Collagen type I (Col I), Collagen type Ⅲ (Col Ⅲ), and Tenascin C (TnC).

View Article and Find Full Text PDF

Background: Cardiac ischemia reperfusion (I/R) injury is a serious consequence of reperfusion therapy for myocardial infarction (MI). Peptidylarginine deiminase 4 (PAD4) is a calcium-dependent enzyme that catalyzes the citrullination of proteins. In previous studies, PAD4 inhibition protected distinct organs from I/R injury by preventing the formation of neutrophil extracellular traps (NETs) and attenuating inflammatory responses.

View Article and Find Full Text PDF

Neuroinflammation within the central nervous system (CNS) is recognized as a critical pathological process in meningitic Escherichia coli (E. coli) infection, leading to severe neurodegenerative disorders and long-term sequelae. Astrocyte reactivity plays a pivotal role in driving the neuroinflammatory cascade in response to pathological stimuli from peripheral sources or other cellular components of the CNS.

View Article and Find Full Text PDF

and Pall. are traditionally used to manage cardiovascular health. However, clinical evidence evaluating standardized extracts for specific cardiovascular benefits is still evolving.

View Article and Find Full Text PDF