scholarly journals Role of Cystathionineγ-Lyase/Hydrogen Sulfide Pathway in Cardiovascular Disease: A Novel Therapeutic Strategy?

2012 ◽  
Vol 17 (1) ◽  
pp. 106-118 ◽  
Author(s):  
Li Long Pan ◽  
Xin Hua Liu ◽  
Qi Hai Gong ◽  
He Bei Yang ◽  
Yi Zhun Zhu
Keyword(s):  
Cardiovascular Disease ◽  
Hydrogen Sulfide ◽  
Therapeutic Strategy ◽  
Novel Therapeutic

Hydrogen sulfide-mediated cardioprotection: mechanisms and therapeutic potential

2010 ◽  
Vol 120 (6) ◽  
pp. 219-229 ◽  
Author(s):  
Madhav Lavu ◽  
Shashi Bhushan ◽  
David J. Lefer
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Hydrogen Sulfide ◽  
Therapeutic Potential ◽  
Blood Pressure Regulation ◽  
Pressure Regulation ◽  
Signalling Molecule ◽  
Anti Inflammatory ◽  
Antioxidant Effects

H2S (hydrogen sulfide), viewed with dread for more than 300 years, is rapidly becoming a ubiquitously present and physiologically relevant signalling molecule. Knowledge of the production and metabolism of H2S has spurred interest in delineating its functions both in physiology and pathophysiology of disease. Although its role in blood pressure regulation and interaction with NO is controversial, H2S, through its anti-apoptotic, anti-inflammatory and antioxidant effects, has demonstrated significant cardioprotection. As a result, a number of sulfide-donor drugs, including garlic-derived polysulfides, are currently being designed and investigated for the treatment of cardiovascular conditions, specifically myocardial ischaemic disease. However, huge gaps remain in our knowledge about this gasotransmitter. Only by additional studies will we understand more about the role of this intriguing molecule in the treatment of cardiovascular disease.

scholarly journals Mitochondrial Function, Biology, and Role in Disease

2016 ◽  
Vol 118 (12) ◽  
pp. 1960-1991 ◽  
Author(s):  
Elizabeth Murphy ◽  
Hossein Ardehali ◽  
Robert S. Balaban ◽  
Fabio DiLisa ◽  
Gerald W. Dorn ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Mitochondrial Function ◽  
The United States ◽  
Therapeutic Interventions ◽  
Therapeutic Approaches ◽  
Mitochondrial Defects ◽  
Exciting Time ◽  
Insight Into ◽  
Novel Therapeutic

Cardiovascular disease is a major leading cause of morbidity and mortality in the United States and elsewhere. Alterations in mitochondrial function are increasingly being recognized as a contributing factor in myocardial infarction and in patients presenting with cardiomyopathy. Recent understanding of the complex interaction of the mitochondria in regulating metabolism and cell death can provide novel insight and therapeutic targets. The purpose of this statement is to better define the potential role of mitochondria in the genesis of cardiovascular disease such as ischemia and heart failure. To accomplish this, we will define the key mitochondrial processes that play a role in cardiovascular disease that are potential targets for novel therapeutic interventions. This is an exciting time in mitochondrial research. The past decade has provided novel insight into the role of mitochondria function and their importance in complex diseases. This statement will define the key roles that mitochondria play in cardiovascular physiology and disease and provide insight into how mitochondrial defects can contribute to cardiovascular disease; it will also discuss potential biomarkers of mitochondrial disease and suggest potential novel therapeutic approaches.

Glucocorticoids and insulin resistance: old hormones, new targets

1999 ◽  
Vol 96 (5) ◽  
pp. 513-523 ◽  
Author(s):  
Robert C. ANDREWS ◽  
Brian R. WALKER
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Cardiovascular Disease ◽  
Cardiovascular Risk ◽  
Insulin Sensitivity ◽  
Cardiovascular Risk Factors ◽  
Therapeutic Strategy ◽  
Clinical Syndrome ◽  
Glucocorticoid Action ◽  
Novel Therapeutic

Insulin resistance has been proposed as a mediator of the association between risk factors for cardiovascular disease in the population. The clinical syndrome of glucocorticoid excess (Cushing's syndrome) is associated with glucose intolerance, obesity and hypertension. By opposing the actions of insulin, glucocorticoids could contribute to insulin resistance and its association with other cardiovascular risk factors. In this review, we describe briefly the known mechanisms of insulin resistance and highlight the potential mechanisms for the effect of glucocorticoids. We then discuss factors which modulate the influence of glucocorticoids on insulin sensitivity; this highlights a novel therapeutic strategy to manipulate glucocorticoid action which may prove to be a useful tool in treating subjects with insulin resistance. Finally, we describe evidence from human studies that glucocorticoids make an important contribution to the pathophysiology of insulin resistance in the population.

The Role of Vascular Cell Senescence in Atherosclerosis: Antisenescence as a Novel Therapeutic Strategy for Vascular Aging

2004 ◽  
Vol 2 (2) ◽  
pp. 141-148 ◽  
Author(s):  
Tohru Minamino ◽  
Hideyuki Miyauchi ◽  
Toshihiko Yoshida ◽  
Kaoru Tateno ◽  
Issei Komuro
Keyword(s):  
Therapeutic Strategy ◽  
Cell Senescence ◽  
Vascular Aging ◽  
Vascular Cell ◽  
Novel Therapeutic ◽  
Vascular Cell Senescence

Effect of SSH1/SSH2 expression changes by shRNA in glioma cell lines on response to radiotherapy and cofilin-1 reactivation.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e13505-e13505
Author(s):  
Hong Xiao
Keyword(s):  
Protein Phosphatase ◽  
Glioma Cell ◽  
Therapeutic Strategy ◽  
Glioma Cells ◽  
Protein Phosphatase 1 ◽  
Migration And Invasion ◽  
Radiation Induced ◽  
U373 Cells ◽  
Novel Therapeutic

e13505 Background: Radiotherapy has become the most important treatment for malignant glioma following surgery. However, development of radioresistance in glioma cells limits therapeutic efficacy. The slingshot (SSH) family of phosphatases is a potent regulator of Cofilin-1 activation. Methods: We investigate the role of SSH1(slingshot protein phosphatase 1) and SSH2 in radioresistance via using shRNA to block SSH1/2 expression in U251 and U373 cells as well as established radioresistant U251 (RR-U251) and U373 (RR-U373) cells. Results: We found that both SSH1 and SSH2-shRNA efficiently sensitized glioma cells to radiation with a sensitization enhancement ratio (SER) of 1.01-1.73. In SSH1-silenced cells, the cell viability, migration, and invasion abilities following radiation were remarkably reduced and radiation induced cell apoptosis was markedly enhanced compared with control cells. While in SSH2-silenced cells, the alterations were not as significant. Furthermore, the result of Western-blot suggested that radiosensization of SSH1/SSH2 silencing was mediated by inhibiting reactivation of phosphorylated CFL-1. Conclusions: Our study demonstrated that SSH1 and SSH2 are valid radiosensitizing targets in not only normal glioma cells but radioresistant lines, suggesting a novel therapeutic strategy to improve the efficacy of radiotherapy in patients with glioma.

scholarly journals Targeting hypoxia in tumor: a new promising therapeutic strategy

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Maria Carla Bosco ◽  
Gabriella D’Orazi ◽  
Donatella Del Bufalo
Keyword(s):  
Cardiovascular Disease ◽  
Therapeutic Strategy ◽  
Metabolic Diseases ◽  
Therapeutic Strategies ◽  
Low Oxygen ◽  
Radio Therapy ◽  
Oxygen Condition ◽  
Negative Role ◽  
Patient Prognosis

AbstractLow oxygen condition (hypoxia) is considered a hallmark of rapidly growing solid tumors. The presence of hypoxia renders tumor cells resistant to conventional chemo- and radio-therapy, selecting a more malignant and invasive phenotype and playing a negative role in patient prognosis. This commentary wishes to recognize the 2019 Nobel Prize in Medicine awarded to three physicians-scientists, Prof. William G. Kaelin Jr., Prof. Sir Peter J. Ratcliffe, and Prof. Gregg L. Semenza, for their discovery of the mechanisms mediating cell ability to sense and adapt to changes in oxygen availability. Their studies established the basis for our understanding of the role of hypoxia in a variety of diseases, including anemia, renal failure, cardiovascular disease, metabolic diseases, and cancer, paving the way for new promising therapeutic strategies through the development of drugs that can either activate or block the oxygen-sensing machinery.

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