scholarly journals The role of matrix metalloproteinases induced angiogenesis during transition from compensatory cardiac hypertrophy to cardiac failure : therapeutic effects of hydrogen sulfide.

2010 ◽  
Author(s):  
Srikanth Givvimani
Keyword(s):  
Hydrogen Sulfide ◽  
Matrix Metalloproteinases ◽  
Cardiac Hypertrophy ◽  
Cardiac Failure ◽  
Therapeutic Effects

scholarly journals MATRIX METALLOPROTEINASES AS MARKERS OF RESPIRATORY TRACT REMODELING AND POTENTIAL THERAPEUTIC TARGET IN PATIENTS WITH BRONCHIAL ASTHMA

2021 ◽  
Vol 9 (2) ◽  
pp. 174-188
Author(s):  
Vladyslava V. Kachkovska
Keyword(s):  
Matrix Metalloproteinases ◽  
Matrix Metalloproteinase ◽  
Bronchial Asthma ◽  
Airway Remodeling ◽  
Matrix Metalloproteinase 9 ◽  
Bronchial Obstruction ◽  
Therapeutic Effects ◽  
External Respiration ◽  
Metalloproteinase 9

It is evidently known that chronic inflammatory process in the bronchi of patients with bronchial asthma is associated with the emergence and progression of airway remodeling, resulting in irreversible obstruction. However, the exact mechanisms of connection between inflammation and airway remodeling are not very well understood and that is the reason for delay of development new specific targeted drugs aimed to inhibit the process of inflammation and remodeling. Therefore, our goal was aimed to analyze and systematize data on the role of matrix metalloproteinases in the occurrence of airway remodeling in patients with bronchial asthma and the possibility of therapeutic effects on this process. Materials and methods: search for information on the role and mechanisms of influence of matrix metalloproteinases on airway remodeling processes in patients with bronchial asthma and the possibility of its pharmacological correction in electronic databases such as PubMed and Google Scholar over the past 25 years. Matrix metalloproteinase-9 and tissue proteinase-1 inhibitor have been shown to play the most important role in airway remodeling in the presence of bronchial asthma, supported by numerous experimental and clinical studies. Much attention is paid to the comparison of these indicators in bronchoalveolar lavage, induced sputum and blood on the background of exacerbation and in the presence of a stable course of the disease. The analysis of their content depending on the severity of the course, dysfunction of external respiration and the degree of reversibility of bronchial obstruction. Studies of the possibility of drug effects on the content of remodeling markers have shown low clinical efficacy. The results are contradictory, but most of them prove the important role of matrix metalloproteinase-9, tissue protease inhibitor-1 and their relationship in the occurrence and progression of airway remodeling and, consequently, the severity of the disease, which dictates the need to develop new additional treatments.

scholarly journals Novel Therapeutic Effects of Pterosin B on Ang II-Induced Cardiomyocyte Hypertrophy

Molecules ◽  
2020 ◽  
Vol 25 (22) ◽  
pp. 5279
Author(s):  
Chang Youn Lee ◽  
Han Ki Park ◽  
Bok-Sim Lee ◽  
Seongtae Jeong ◽  
Sung-Ae Hyun ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Protective Role ◽  
Cardiomyocyte Hypertrophy ◽  
Therapeutic Effects ◽  
Ang Ii ◽  
Pathological Cardiac Hypertrophy ◽  
Glycation End Products ◽  
Abnormal Increase

Pathological cardiac hypertrophy is characterized by an abnormal increase in cardiac muscle mass in the left ventricle, resulting in cardiac dysfunction. Although various therapeutic approaches are being continuously developed for heart failure, several studies have suggested natural compounds as novel potential strategies. Considering relevant compounds, we investigated a new role for Pterosin B for which the potential life-affecting biological and therapeutic effects on cardiomyocyte hypertrophy are not fully known. Thus, we investigated whether Pterosin B can regulate cardiomyocyte hypertrophy induced by angiotensin II (Ang II) using H9c2 cells. The antihypertrophic effect of Pterosin B was evaluated, and the results showed that it reduced hypertrophy-related gene expression, cell size, and protein synthesis. In addition, upon Ang II stimulation, Pterosin B attenuated the activation and expression of major receptors, Ang II type 1 receptor and a receptor for advanced glycation end products, by inhibiting the phosphorylation of PKC-ERK-NF-κB pathway signaling molecules. In addition, Pterosin B showed the ability to reduce excessive intracellular reactive oxygen species, critical mediators for cardiac hypertrophy upon Ang II exposure, by regulating the expression levels of NAD(P)H oxidase 2/4. Our results demonstrate the protective role of Pterosin B in cardiomyocyte hypertrophy, suggesting it is a potential therapeutic candidate.

scholarly journals Matrix metalloproteinases in atherosclerosis: role of nitric oxide, hydrogen sulfide, homocysteine, and polymorphisms

2015 ◽  
pp. 173 ◽  
Author(s):  
Thomas Vacek ◽  
Shahnaz Rahman ◽  
Shipeng Yu ◽  
Diana Neamtu ◽  
Srikanth Givimani ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Matrix Metalloproteinases

scholarly journals NLRP3-mediated pyroptosis aggravates pressure overload-induced cardiac hypertrophy, fibrosis, and dysfunction in mice: cardioprotective role of irisin

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Rongchuan Yue ◽  
Zaiyong Zheng ◽  
Yu Luo ◽  
Xiaobo Wang ◽  
Mingming Lv ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Nlrp3 Inflammasome ◽  
Critical Role ◽  
Pressure Overload ◽  
Receptor Protein ◽  
Therapeutic Effects ◽  
Aortic Constriction ◽  
Cardioprotective Effects ◽  
Promising Therapeutic Agent

AbstractThe exact mechanism of myocardial hypertrophy has not been completely elucidated. NOD-like receptor protein 3 (NLRP3) and the pyroptotic cascade play a critical role in cardiac hypertrophy and inflammation. The myokine irisin can inhibit NLRP3 activation, although its exact mechanism of action is unknown. In this study, we induced cardiac hypertrophy in a mouse model via aortic constriction (TAC) to further explore the pathological role of NLRP3 inflammasome-mediated pyroptosis and the potential therapeutic effects of irisin. Cardiac hypertrophy significantly increased the percentage of apoptotic cells and upregulated IL-1β, cleaved caspase-1, and GSDMD-N that lie downstream of the NLRP3 inflammasome. Subsequently, irisin was co-administered to the TAC mice or angiotensin II (Ang-II)-treated cardiomyocytes to observe whether it could attenuate pyroptosis and cardiac hypertrophy. We established a direct association between pyroptosis and cardiac hypertrophy and found that pharmacological or genetic inhibition of NLRP3 attenuated cardiac hypertrophy. Furthermore, ectopic overexpression of NLRP3 abrogated the cardioprotective effects of irisin. To summarize, pyroptosis is a pathological factor in cardiac hypertrophy, and irisin is a promising therapeutic agent that inhibits NLRP3-mediated pyroptosis of cardiomyocytes.

The Role of Reactive Oxygen Species, Kinases, Hydrogen Sulfide, and Nitric Oxide in the Regulation of Autophagy and Their Impact on Ischemia and Reperfusion Injury in the Heart

2020 ◽  
Vol 16 ◽  
Author(s):  
Andrey Krylatov ◽  
Leonid Maslov ◽  
Sergey Y. Tsibulnikov ◽  
Nikita Voronkov ◽  
Alla Boshchenko ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Hydrogen Sulfide ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Ischemia And Reperfusion ◽  
Oxygen Species ◽  
Ischemia And Reperfusion Injury ◽  
Adaptive Process

: There is considerable evidence in the heart that autophagy in cardiomyocytes is activated by hypoxia/reoxygenation (H/R) or in hearts by ischemia/reperfusion (I/R). Depending upon the experimental model and duration of ischemia, increases in autophagy in this setting maybe beneficial (cardioprotective) or deleterious (exacerbate I/R injury). Aside from the conundrum as to whether or not autophagy is an adaptive process, it is clearly regulated by a number of diverse molecules including reactive oxygen species (ROS), various kinases, hydrogen sulfide (H2S) and nitric oxide (NO). The purpose this review is to address briefly the controversy regarding the role of autophagy in this setting and to examine a variety of disparate molecules that are involved in its regulation.

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