scholarly journals Sex Differences and Regulatory Actions of Estrogen in Cardiovascular System

2021 ◽  
Vol 12 ◽  
Author(s):  
Kazutaka Ueda ◽  
Nobuaki Fukuma ◽  
Yusuke Adachi ◽  
Genri Numata ◽  
Hiroyuki Tokiwa ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sex Differences ◽  
Hormone Replacement ◽  
Tissue Homeostasis ◽  
Cardiovascular Tissue ◽  
Full Extent ◽  
Great Progress ◽  
Regulatory Actions ◽  
Made In

Great progress has been made in the understanding of the pathophysiology of cardiovascular diseases (CVDs), and this has improved the prevention and prognosis of CVDs. However, while sex differences in CVDs have been well documented and studied for decades, their full extent remains unclear. Results of the latest clinical studies provide strong evidence of sex differences in the efficacy of drug treatment for heart failure, thereby possibly providing new mechanistic insights into sex differences in CVDs. In this review, we discuss the significance of sex differences, as rediscovered by recent studies, in the pathogenesis of CVDs. First, we provide an overview of the results of clinical trials to date regarding sex differences and hormone replacement therapy. Then, we discuss the role of sex differences in the maintenance and disruption of cardiovascular tissue homeostasis.

scholarly journals Update in Endocrine Autoimmunity

2008 ◽  
Vol 93 (10) ◽  
pp. 3663-3670 ◽  
Author(s):  
Mark S. Anderson
Keyword(s):  
Autoimmune Diseases ◽  
Hormone Replacement ◽  
Endocrine System ◽  
Human Leukocyte ◽  
Endocrine Disorders ◽  
Autoimmune Polyglandular Syndrome ◽  
New Genes ◽  
Autoimmune Polyglandular Syndrome Type ◽  
Made In

Context: The endocrine system is a common target in pathogenic autoimmune responses, and there has been recent progress in our understanding, diagnosis, and treatment of autoimmune endocrine diseases. Synthesis: Rapid progress has recently been made in our understanding of the genetic factors involved in endocrine autoimmune diseases. Studies on monogenic autoimmune diseases that include endocrine phenotypes like autoimmune polyglandular syndrome type 1 and immune dysregulation, polyendocrinopathy, enteropathy, X-linked have helped reveal the role of key regulators in the maintenance of immune tolerance. Highly powered genetic studies have found and confirmed many new genes outside of the established role of the human leukocyte antigen locus with these diseases, and indicate an essential role of immune response pathways in these diseases. Progress has also been made in identifying new autoantigens and the development of new animal models for the study of endocrine autoimmunity. Finally, although hormone replacement therapy is still likely to be a mainstay of treatment in these disorders, there are new agents being tested for potentially treating and reversing the underlying autoimmune process. Conclusion: Although autoimmune endocrine disorders are complex in etiology, these recent advances should help contribute to improved outcomes for patients with, or at risk for, these disorders.

Protective effect of melatonin in atherosclerotic cardiovascular disease: A comprehensive review

2021 ◽  
Vol 4 (3) ◽  
pp. 408-430
Author(s):  
Madhuri Datta ◽  
Romit Majumder ◽  
Aindrila Chattopadhyay ◽  
Debasish Bandyopadhyay
Keyword(s):  
Heart Failure ◽  
Conventional Therapy ◽  
Death Rate ◽  
Synergistic Effects ◽  
Atherosclerotic Cardiovascular Disease ◽  
Comprehensive Review ◽  
Cardiovascular Tissue ◽  
Pathological Conditions ◽  
Heart Disorders

Heart failure is characterized by the heart losing its capacity to pump sufficient blood to match the body’s demand. It is caused by  a variety of cardiovascular impairments. Among them,  atherosclerosis is the most common one. Although, a variety of medicines selectively target this pathology, the death rate due to atherosclerosis associated heart disorders remain high. To address this issue,  the use of antioxidants combined with conventional therapy to achieve synergistic effects has gained popularity. Melatonin is one of such antioxidants. In addition to its potent antioxidant activity, this molecule acts in harmony to protect the cardiovascular tissue. This review explores the various mechanisms by which melatonin protects the cardiovascular tissue. This information will contribute further insights into the role of melatonin in maintaining cardiovascular homeostasis in normal as well as in pathological conditions. It will also help us to better understand the potential synergistic effects of melatonin with conventional therapy to successfully target the heart failure associated with atherosclerosis.  

scholarly journals Progress in experimental research on SPRED protein family

2020 ◽  
Vol 48 (8) ◽  
pp. 030006052092917
Author(s):  
Jian Gong ◽  
Zhangren Yan ◽  
Qiao Liu
Keyword(s):  
Tumor Metastasis ◽  
Experimental Studies ◽  
Erk Signaling ◽  
Allergic Reactions ◽  
Great Progress ◽  
Ophthalmic Diseases ◽  
Hematopoietic Regulation ◽  
Development Movement ◽  
Made In

The Sprouty-related Ena/vasodilator-stimulated phosphoprotein homology-1 (EVH-1) domain (SPRED) family of proteins was discovered in 2001. These Sprouty-related tyrosine kinase-binding proteins negatively regulate a variety of growth factor-induced Ras/ERK signaling pathways. In recent years, SPRED proteins have been found to regulate vital activities such as cell development, movement, and proliferation, and to participate in pathophysiological processes such as tumor metastasis, hematopoietic regulation, and allergic reactions. The findings of these studies have important implications regarding the involvement of SPRED proteins in disease. Early studies of SPRED proteins focused mainly on various tumors, cardiovascular diseases, and organ development. However, in recent years, great progress has been made in elucidating the role of SPRED proteins in neuropsychiatric, inflammatory, endocrine, and ophthalmic diseases. This article provides a review of the experimental studies performed in recent years on the SPRED proteins and their role in the pathogenesis of certain diseases.

STAT signalling in the heart and cardioprotection

2006 ◽  
Vol 8 (15) ◽  
pp. 1-16 ◽  
Author(s):  
Surinder M. Soond ◽  
David S. Latchman ◽  
Anastasis Stephanou
Keyword(s):  
Cardiac Myocyte ◽  
Signalling Pathways ◽  
Janus Kinases ◽  
Signal Transducers ◽  
The Past ◽  
Ischaemia Reperfusion ◽  
Myocardial Preconditioning ◽  
Great Progress ◽  
Made In

During the past six years, great progress has been made in defining the key cellular and molecular signalling pathways that determine the fate of cardiac myocytes after ischaemia–reperfusion (IR) and consequently the severity of myocardial infarction. Among the complex network of kinases and transcription factors that mediate signals during IR is the STAT family of ‘signal transducers and activators of transcription’. During IR they are inducibly activated by Janus kinases and have the capability of transcriptionally regulating pro-survival and apoptotic gene expression. In this review we focus on recent progress made in elucidating the regulation and role of the STAT family of proteins during cardioprotective signalling events in myocardial preconditioning and during IR injury in cardiac myocyte cells and the myocardium. Moreover, we also highlight developments in understanding how this signalling pathway might be amenable to therapeutic intervention, permitting cardiac myocyte survival following IR.

Protective role of peroxiredoxin-4 in heart failure

2020 ◽  
Vol 134 (1) ◽  
pp. 71-72
Author(s):  
Naseer Ahmed ◽  
Masooma Naseem ◽  
Javeria Farooq
Keyword(s):  
Heart Failure ◽  
Cardiac Fibroblasts ◽  
Protective Role ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Galectin 3 ◽  
Consequent Increase ◽  
And Oxidative Stress

Abstract Recently, we have read with great interest the article published by Ibarrola et al. (Clin. Sci. (Lond.) (2018) 132, 1471–1485), which used proteomics and immunodetection methods to show that Galectin-3 (Gal-3) down-regulated the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts. Authors concluded that ‘antioxidant activity of Prx-4 had been identified as a protein down-regulated by Gal-3. Moreover, Gal-3 induced a decrease in total antioxidant capacity which resulted in a consequent increase in peroxide levels and oxidative stress markers in cardiac fibroblasts.’ We would like to point out some results stated in the article that need further investigation and more detailed discussion to clarify certain factors involved in the protective role of Prx-4 in heart failure.

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