Nanomedicine has elegantly attempted to cure multiple gene polymorphisms and mutations in cardiovascular diseases using gene therapy techniques.

2021 ◽  
Author(s):  
Moataz Dowaidar
Keyword(s):  
Gene Therapy ◽  
Heart Disease ◽  
Cardiovascular Diseases ◽  
Gene Polymorphisms ◽  
Distribution Systems ◽  
Genetic Factors ◽  
Multiple Gene ◽  
Complex Interactions ◽  
Direct Delivery ◽  
Vector Delivery

The molecular mediators that induce MI, the loss of myocardial regeneration, and the development of heart disease are all being researched more thoroughly. It's intriguing to think about how genetic factors could be used to modulate these disease mediators. DNA, RNA, or proteins may both be included in this operation. However, direct delivery of these biomolecules is not always effective. Using gene therapy methods, nanomedicine has elegantly attempted to reverse many gene polymorphisms and defects in complex diseases.The stability of these biomolecules, as well as their controlled release and passage through barriers to the operating site, can be aided by delivery systems. Precision-tailored vector delivery has been shown to reduce toxicity and improve drug availability. Currently, a variety of distribution systems are being evaluated, with the frontrunners incorporating security and conclusions being selected.New biological mediators, as well as the complex interactions within them, as well as their pharmacokinetic and pharmacodynamic profiles, will be discovered in the future. This opens the door to a more advanced delivery system that meets the biological requirements for maximum therapeutic efficacy.

Молекулярная биология менингиом головного мозга

2017 ◽  
pp. 82-91
Author(s):  
В.А. Бывальцев ◽  
И.А. Степанов ◽  
Е.Г. Белых ◽  
А.И. Яруллина
Keyword(s):  
Gene Therapy ◽  
Proton Therapy ◽  
Genetic Factors ◽  
Intracranial Tumor ◽  
Molecular Profile ◽  
Genetic Changes ◽  
Treatment Techniques ◽  
Downstream Effects ◽  
Si Rna ◽  
The Relationship

Цель обзора - анализ современных данных литературы о нарушении внутриклеточных сигнальных путей, играющих ведущую роль в развитии менингиом, генетических и молекулярных профилях данной группы опухолей. К настоящему времени изучено множество аберрантных сигнальных внутриклеточных путей, которые играют важнейшую роль в развитии менингиом головного мозга. Четкое понимание поврежденных внутриклеточных каскадов поможет изучить влияние генетических мутаций и их эффектов на менингиомогенез. Подробное исследование генетического и молекулярного профиля менингиом позволит сделать первый уверенный шаг в разработке более эффективных методов лечения данной группы интракраниальных опухолей. Хромосомы 1, 10, 14, 22 и связанные с ними генные мутации ответственны за рост и прогрессию менингиом. Предполагается, что только через понимание данных генетических повреждений будут реализованы новейшие эффективные методы лечения. Будущая терапия будет включать в себя комбинации таргетных молекулярных агентов, в том числе генную терапию, малые интерферирующие РНК, протонную терапию и другие методы воздействия, как результат дальнейшего изучения генетических и биологических изменений, характерных для менингеальных опухолей. Meningiomas are by far the most common tumors arising from the meninges. A myriad of aberrant signaling pathways involved with meningioma tumorigenesis, have been discovered. Understanding these disrupted pathways will aid in deciphering the relationship between various genetic changes and their downstream effects on meningioma pathogenesis. An understanding of the genetic and molecular profile of meningioma would provide a valuable first step towards developing more effective treatments for this intracranial tumor. Chromosomes 1, 10, 14, 22, their associated genes, have been linked to meningioma proliferation and progression. It is presumed that through an understanding of these genetic factors, more educated meningioma treatment techniques can be implemented. Future therapies will include combinations of targeted molecular agents including gene therapy, si-RNA mediation, proton therapy, and other approaches as a result of continued progress in the understanding of genetic and biological changes associated with meningiomas.

scholarly journals The clinical value of ficolin-3 gene polymorphism in rheumatic heart disease. An Egyptian adolescents study

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Maher H. Gomaa ◽  
Emad Gamil Khidr ◽  
Ahmed Elshafei ◽  
Hala S. Hamza ◽  
Aya M. Fattouh ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Heart Disease ◽  
Gene Polymorphism ◽  
Rheumatic Heart Disease ◽  
Streptococcus Pyogenes ◽  
Gene Polymorphisms ◽  
Clinical Value ◽  
Homozygous Genotype ◽  
First Time ◽  
Rheumatic Heart

Abstract Objective Ficolin-3 is one of the innate immunity molecules that was thought to play a pivotal role in Streptococcus pyogenes autoimmunity and its complications; rheumatic fever (RF) and rheumatic heart disease (RHD). We aimed to disclose if there is an association between ficolin-3 (FCN3) gene polymorphisms (rs4494157 and rs10794501) and RF with or without RHD for the first time in Egyptian adolescents. Results Serum ficolin-3 level was significantly elevated in patients suffering from RF with and without RHD in comparison with control. Regarding FCN3 gene (rs4494157) polymorphism, a significant correlation was found between the A allele and the susceptibility to RF with or without RHD (OR = 2.93, P = 0.0002 and OR = 2.23, P = 0.008 respectively). Besides, AA homozygous genotype showed a significant association with RHD risk (OR = 3.47, P = 0.026). Patients carrying the A allele (CA + AA) had significantly higher serum ficolin-3 than those carrying the CC genotype (P ˂ 0.0001). While the frequency of (rs10794501) polymorphism revealed no significant differences between the controls and RF patients with or without RHD (OR = 1.43, P = 0.261 and OR = 1.48, P = 0.208 respectively).

scholarly journals Renin-angiotensin system gene polymorphisms and premature coronary heart disease

2005 ◽  
Vol 6 (1) ◽  
pp. 38-42 ◽  
Author(s):  
Cevad Sekuri ◽  
F Sirri Cam ◽  
Ertugrul Ercan ◽  
Istemihan Tengiz ◽  
Abdi Sagcan ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Gene Polymorphisms ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Premature Coronary Heart Disease

Gene Therapy in Cardiovascular Diseases

2002 ◽  
Vol 2 (4) ◽  
pp. 427-435 ◽  
Author(s):  
Kamala Tamirisa ◽  
Debabrata Mukherjee
Keyword(s):  
Gene Therapy ◽  
Cardiovascular Diseases

Prediction of atherosclerosis in children and the possibility of early prevention of coronary heart disease

1999 ◽  
Vol 80 (4) ◽  
pp. 296-297
Author(s):  
O. I. Pikuza ◽  
V. N. Oslopov ◽  
H. M. Vakhitov ◽  
A. A. Babushkina ◽  
S. E. Nikolsky
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Coronary Artery ◽  
Cardiovascular Diseases ◽  
Childhood And Adolescence ◽  
Early Prevention ◽  
Cerebrovascular Pathology ◽  
Artery Disease

Cardiovascular diseases caused by atherosclerosis (coronary artery disease, cerebrovascular pathology, etc.) are responsible for 40-50% of all deaths in adults. Of particular concern to clinicians is the emerging unfavorable tendency to "rejuvenate" these diseases. Currently, the fact that atherosclerosis (AS) begins to form in childhood and adolescence is indisputable.

Highlighting Exosomes' Function in Cardiovascular Diseases

2021 ◽  
Vol 17 ◽  
Author(s):  
Sidhi Laksono ◽  
Budhi Setianto ◽  
Ananta Siddhi Prawara ◽  
Bambang Dwiputra
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Heart Disease ◽  
Cardiovascular Diseases ◽  
Prognostic Marker ◽  
Therapeutic Agent ◽  
Diagnostic Marker ◽  
Cell Communication ◽  
Surface Protein ◽  
Cardiovascular Patients

: Exosomes as one of the extracellular vesicles’ subgroups played an important role in the cell to cell communication. The cargos and surface protein of exosomes have been known to affect the cardiovascular system both positively and negatively in chronic heart failure, ischemic heart disease, and atherosclerosis. There have been several exosomes that emerged as a potential diagnostic and prognostic marker in cardiovascular patients. However, the conditions affecting the patients and the method of isolation should be considered to create a standardized normal value of the exosomes and the components. CPC-derived exosomes, ADSCs-derived exosomes, and telocyte-derived exosomes have been proven to be capable ofacting as a therapeutic agent in myocardial infarction models. Exosomes have the potential to become a diagnostic marker, prognostic marker, and therapeutic agent in cardiovascular diseases.

scholarly journals Association of Cystathionine β-Synthase Gene Polymorphisms With Preeclampsia

2018 ◽  
Vol 24 (9_suppl) ◽  
pp. 285S-293S ◽  
Author(s):  
Mercedes Piedad de León Bautista ◽  
Mirza Romero-Valdovinos ◽  
Beatriz Zavaleta-Villa ◽  
Arony Martínez-Flores ◽  
Angélica Olivo-Díaz
Keyword(s):  
Risk Factor ◽  
Cardiovascular Diseases ◽  
Base Pair ◽  
Gene Polymorphisms ◽  
Case Control Study ◽  
High Plasma ◽  
Case Control ◽  
Related Factor ◽  
Mexican Women ◽  
Control Study

Preeclampsia (PE) is a pregnancy disorder that increases maternal and fetal morbidity and mortality worldwide. High plasma levels of homocysteine (Hcy) are a risk factor for several cardiovascular diseases. Cystathionine β-synthase (CBS) plays an important role in Hcy homeostasis catalyzing the irreversible degradation of Hcy to cystathionine, protecting the endothelium from injury caused by hypoxia. Several mutations and polymorphisms may alter the expression of the CBS gene, resulting in variable levels of Hcy. The purpose of this study was to investigate the association of CBS gene polymorphisms with PE in Mexican women. A case–control study consisting of 129 pregnant women with PE (37 severe and 92 mild) and 173 women with uncomplicated pregnancies was performed. Polymorphisms, such as G797A, C785T, T833C, G919A, T959C, C1105T, and 844ins68 base pair, in the CBS gene were genotyped. The polymorphism G797A was monomorphic in cases with the presence of only G797A-G allele. Allele C785T-T and genotype C785T-C/T were associated with susceptibility in severe and mild PE. Alleles G797A-G and T959C-T were associated with susceptibility only in severe PE. Haplotype TGTWGTC was of susceptibility for severe PE and of protection for mild PE. Haplotypes CGTWGCC and CATWGTC seem to be protective for severe PE, but the latter is related to susceptibility in mild PE. The results suggest that C785T, G797A, and T959C mutations are contributing in different ways in severe and mild PE in our population and could be count as another related factor for this disease.

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