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1.
Artigo em Inglês | MEDLINE | ID: mdl-29886837

RESUMO

BACKGROUND: Cardiovascular diseases such as endocarditis are the second most common cause of death worldwide. Infective Endocarditis (IE) is the most severe infection of the heart associated with significant mortality and morbidity. The binding and invasion of Human Aortic Endothelial Cells (HAECs) by pathogenic microbes can play an important role in the pathogenesis of IE. OBJECTIVE: Pseudomonas aeruginosa is an emerging pathogen that has been associated with IE. However, it is not known whether P. aeruginosa can bind and interact with HAECs. The aim of this study was to determine whether P. aeruginosa can bind and colonize HAECs. METHODS: The invasion of HAECs by P. aeruginosa was assessed by gentamicin protection assay. Cytokine levels were determined by enzyme-linked Immunosorbent Assay (ELISA) kits. Cell damage was determined by Lactate Dehydrogenase (LDH) assay. RESULTS: P. aeruginosa can bind and invade HAECs. Infection of HAECs with P. aeruginosa induces TNF-α IL-1ß, IL-6 and IL-8 cytokine production leading to the generation of inflammatory milieu that can cause tissue damage as observed in human clinical cases of IE. We also observed that P. aeruginosa induces cell damage in HAECs. CONCLUSION: In this study, we demonstrate for first time that P. aeruginosa can invade and survive inside HAECs. This cell culture model can be of immense importance to determine the efficacy of drug targets against IE.


Assuntos
Morte Celular/imunologia , Endocardite/fisiopatologia , Células Endoteliais/microbiologia , Pseudomonas aeruginosa/patogenicidade , Humanos
2.
Artigo em Inglês | MEDLINE | ID: mdl-29737266

RESUMO

Cardiovascular Diseases (CVDs) are a leading cause of morbidity and mortality worldwide. The underlying pathology for cardiovascular disease is largely atherosclerotic in nature and the steps include fatty streak formation, plaque progression and plaque rupture. While there is optimal drug therapy available for patients with CVD, there are also underlying drug delivery obstacles that must be addressed. Challenges in drug delivery warrant further studies for the development of novel and more efficacious medical therapies. An extensive understanding of the molecular mechanisms of disease in combination with current challenges in drug delivery serves as a platform for the development of novel drug therapeutic targets for CVD. The objective of this article is to review the pathogenesis of atherosclerosis, first-line medical treatment for CVD, and key obstacles in an efficient drug delivery.


Assuntos
Aterosclerose/complicações , Doenças Cardiovasculares/patologia , Doenças Cardiovasculares/terapia , Sistemas de Liberação de Medicamentos/métodos , Aterosclerose/patologia , Humanos
3.
Artif Cells Nanomed Biotechnol ; 46(sup1): 831-840, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29447002

RESUMO

Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality worldwide. Due to the significant impact of CVD on humans, there is a need to develop novel treatment modalities tailored to major classes of cardiac diseases including hypertension, coronary artery disease, cardiomyopathies, arrhythmias, valvular disease and inflammatory diseases. In this article, we discuss recent advancements regarding development of therapeutic strategies based on stem cells, aptamers, exosomes, drug-eluting and dissolvable stents, immunotherapy and nanomedicine for the treatment of CVD. We summarize current research and clinical advances in cardiovascular therapeutics, with a focus on therapies that move beyond current oral- or sublingual-based regimens. This review article provides insight into current research and future treatment strategies that hold a great relevance for future clinical practice in pursuit of improving quality of life of patients suffering from CVD.


Assuntos
Aptâmeros de Nucleotídeos/metabolismo , Doenças Cardiovasculares/terapia , Exossomos/metabolismo , Nanomedicina/métodos , Células-Tronco , Animais , Doenças Cardiovasculares/metabolismo , Doenças Cardiovasculares/patologia , Humanos
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