scholarly journals If Channel as an Emerging Therapeutic Target for Cardiovascular Diseases: A Review of Current Evidence and Controversies

2017 ◽  
Vol 8 ◽  
Author(s):  
Hayelom G. Mengesha ◽  
Tadesse B. Tafesse ◽  
Mohammed H. Bule
Keyword(s):  
Cardiovascular Diseases ◽  
Therapeutic Target ◽  
Current Evidence

Protein Kinase C – Possible Therapeutic Target to Treat Cardiovascular Diseases

2010 ◽  
Vol 10 (4) ◽  
pp. 292-308 ◽  
Author(s):  
Yamini S. Bynagari-Settipalli ◽  
Ramya Chari ◽  
Laurie Kilpatrick ◽  
Satya P. Kunapuli
Keyword(s):  
Protein Kinase C ◽  
Cardiovascular Diseases ◽  
Protein Kinase ◽  
Therapeutic Target ◽  
Kinase C

scholarly journals Osteopontin in Cardiovascular Diseases

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1047
Author(s):  
Kohsuke Shirakawa ◽  
Motoaki Sano
Keyword(s):  
Cardiovascular Risk ◽  
Cardiovascular Diseases ◽  
Therapeutic Target ◽  
Gene Mutations ◽  
Major Adverse Cardiovascular Event ◽  
Matricellular Protein ◽  
Pathological State ◽  
Adverse Cardiovascular Event ◽  
Anti Inflammatory

Unprecedented advances in secondary prevention have greatly improved the prognosis of cardiovascular diseases (CVDs); however, CVDs remain a leading cause of death globally. These findings suggest the need to reconsider cardiovascular risk and optimal medical therapy. Numerous studies have shown that inflammation, pro-thrombotic factors, and gene mutations are focused not only on cardiovascular residual risk but also as the next therapeutic target for CVDs. Furthermore, recent clinical trials, such as the Canakinumab Anti-inflammatory Thrombosis Outcomes Study trial, showed the possibility of anti-inflammatory therapy for patients with CVDs. Osteopontin (OPN) is a matricellular protein that mediates diverse biological functions and is involved in a number of pathological states in CVDs. OPN has a two-faced phenotype that is dependent on the pathological state. Acute increases in OPN have protective roles, including wound healing, neovascularization, and amelioration of vascular calcification. By contrast, chronic increases in OPN predict poor prognosis of a major adverse cardiovascular event independent of conventional cardiovascular risk factors. Thus, OPN can be a therapeutic target for CVDs but is not clinically available. In this review, we discuss the role of OPN in the development of CVDs and its potential as a therapeutic target.

scholarly journals Circadian Rhythm: Potential Therapeutic Target for Atherosclerosis and Thrombosis

2021 ◽  
Vol 22 (2) ◽  
pp. 676
Author(s):  
Andy W. C. Man ◽  
Huige Li ◽  
Ning Xia
Keyword(s):  
Circadian Rhythm ◽  
Cardiovascular Diseases ◽  
Circadian Rhythms ◽  
Circadian Clock ◽  
Therapeutic Target ◽  
Environmental Changes ◽  
Clock Genes ◽  
Vascular System ◽  
Peripheral Tissues ◽  
Inflammatory Processes

Every organism has an intrinsic biological rhythm that orchestrates biological processes in adjusting to daily environmental changes. Circadian rhythms are maintained by networks of molecular clocks throughout the core and peripheral tissues, including immune cells, blood vessels, and perivascular adipose tissues. Recent findings have suggested strong correlations between the circadian clock and cardiovascular diseases. Desynchronization between the circadian rhythm and body metabolism contributes to the development of cardiovascular diseases including arteriosclerosis and thrombosis. Circadian rhythms are involved in controlling inflammatory processes and metabolisms, which can influence the pathology of arteriosclerosis and thrombosis. Circadian clock genes are critical in maintaining the robust relationship between diurnal variation and the cardiovascular system. The circadian machinery in the vascular system may be a novel therapeutic target for the prevention and treatment of cardiovascular diseases. The research on circadian rhythms in cardiovascular diseases is still progressing. In this review, we briefly summarize recent studies on circadian rhythms and cardiovascular homeostasis, focusing on the circadian control of inflammatory processes and metabolisms. Based on the recent findings, we discuss the potential target molecules for future therapeutic strategies against cardiovascular diseases by targeting the circadian clock.

scholarly journals The Notch pathway: a novel therapeutic target for cardiovascular diseases?

2019 ◽  
Vol 23 (8) ◽  
pp. 695-710 ◽  
Author(s):  
Giorgio Aquila ◽  
Aleksandra Kostina ◽  
Francesco Vieceli Dalla Sega ◽  
Eugeniy Shlyakhto ◽  
Anna Kostareva ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Therapeutic Target ◽  
Notch Pathway ◽  
Novel Therapeutic

Role of spinal neurons in the maintenance of elevated sympathetic activity: a novel therapeutic target?

2020 ◽  
Vol 319 (3) ◽  
pp. R282-R287
Author(s):  
Maycon I. O. Milanez ◽  
Erika E. Nishi ◽  
Cássia T. Bergamaschi ◽  
Ruy R. Campos
Keyword(s):  
Cardiovascular Diseases ◽  
Therapeutic Target ◽  
Sympathetic Activity ◽  
Spinal Neurons ◽  
Potential Therapeutic Target ◽  
Present Evidence ◽  
Extensive Range ◽  
Vasomotor Activity ◽  
The Brain

The control of sympathetic vasomotor activity involves a complex network within the brain and spinal circuits. An extensive range of studies has indicated that sympathoexcitation is a common feature in several cardiovascular diseases and that strategies to reduce sympathetic vasomotor overactivity in such conditions can be beneficial. In the present mini-review, we present evidence supporting the spinal cord as a potential therapeutic target to mitigate sympathetic vasomotor overactivity in cardiovascular diseases, focusing mainly on the actions of spinal angiotensin II on the control of sympathetic preganglionic neuronal activity.

scholarly journals Regulation of DDAH1 as a Potential Therapeutic Target for Treating Cardiovascular Diseases

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Xiaoyu Liu ◽  
John Fassett ◽  
Yidong Wei ◽  
Yingjie Chen
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiovascular Diseases ◽  
Therapeutic Target ◽  
Farnesoid X Receptor ◽  
Nitric Oxide Synthase Inhibitor ◽  
Endogenous Nitric Oxide ◽  
Synthase Inhibitor ◽  
Nitric Oxide Bioavailability

Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase inhibitor that blocks nitric oxide production, while congestive heart failure is associated with increased plasma and tissue ADMA content. Increased plasma ADMA is a strong and independent predictor of all-cause mortality in the community and the strongest predictor of mortality in patients after myocardial infarction. Recent studies demonstrated that dimethylarginine dimethylaminohydrolase-1 (DDAH1) is the critical enzyme for ADMA degradation and thereby plays an important role in maintaining cardiovascular nitric oxide bioavailability. Interestingly, activation of the farnesoid X receptor (FXR) through the bile acid ursodeoxycholic acid (UDCA) or synthetic FXR agonists, such as GW4064, can increase DDAH1 expression. Thus, modulating DDAH1 activity through FXR receptor agonists such as UDCA could be a therapeutic target for treating reduced nitric oxide bioavailability in congestive heart failure and other cardiovascular diseases.

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