scholarly journals Sex Hormone Regulation of Proteins Modulating Mitochondrial Metabolism, Dynamics and Inter-Organellar Cross Talk in Cardiovascular Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Shannon Lynch ◽  
James E. Boyett ◽  
M. Ryan Smith ◽  
Samantha Giordano-Mooga
Keyword(s):  
Cardiovascular Disease ◽  
Sex Hormones ◽  
Mitochondrial Biogenesis ◽  
Cross Talk ◽  
Mitochondrial Dynamics ◽  
Sex Hormone ◽  
Regulatory Role ◽  
Future Research ◽  
Hormone Regulation

Cardiovascular disease (CVD) is the leading cause of death in the U.S. and worldwide. Sex-related disparities have been identified in the presentation and incidence rate of CVD. Mitochondrial dysfunction plays a role in both the etiology and pathology of CVD. Recent work has suggested that the sex hormones play a role in regulating mitochondrial dynamics, metabolism, and cross talk with other organelles. Specifically, the female sex hormone, estrogen, has both a direct and an indirect role in regulating mitochondrial biogenesis via PGC-1α, dynamics through Opa1, Mfn1, Mfn2, and Drp1, as well as metabolism and redox signaling through the antioxidant response element. Furthermore, data suggests that testosterone is cardioprotective in males and may regulate mitochondrial biogenesis through PGC-1α and dynamics via Mfn1 and Drp1. These cell-signaling hubs are essential in maintaining mitochondrial integrity and cell viability, ultimately impacting CVD survival. PGC-1α also plays a crucial role in inter-organellar cross talk between the mitochondria and other organelles such as the peroxisome. This inter-organellar signaling is an avenue for ameliorating rampant ROS produced by dysregulated mitochondria and for regulating intrinsic apoptosis by modulating intracellular Ca2+ levels through interactions with the endoplasmic reticulum. There is a need for future research on the regulatory role of the sex hormones, particularly testosterone, and their cardioprotective effects. This review hopes to highlight the regulatory role of sex hormones on mitochondrial signaling and their function in the underlying disparities between men and women in CVD.

scholarly journals Regulatory Role of Sex Hormones in Cardiovascular Calcification

2021 ◽  
Vol 22 (9) ◽  
pp. 4620
Author(s):  
Holly J. Woodward ◽  
Dongxing Zhu ◽  
Patrick W. F. Hadoke ◽  
Victoria E. MacRae
Keyword(s):  
Cardiovascular Disease ◽  
Sex Differences ◽  
Sexual Dimorphism ◽  
Aortic Stenosis ◽  
Sex Hormones ◽  
Sex Hormone ◽  
Increased Risk ◽  
Male Sex ◽  
Primary Male

Sex differences in cardiovascular disease (CVD), including aortic stenosis, atherosclerosis and cardiovascular calcification, are well documented. High levels of testosterone, the primary male sex hormone, are associated with increased risk of cardiovascular calcification, whilst estrogen, the primary female sex hormone, is considered cardioprotective. Current understanding of sexual dimorphism in cardiovascular calcification is still very limited. This review assesses the evidence that the actions of sex hormones influence the development of cardiovascular calcification. We address the current question of whether sex hormones could play a role in the sexual dimorphism seen in cardiovascular calcification, by discussing potential mechanisms of actions of sex hormones and evidence in pre-clinical research. More advanced investigations and understanding of sex hormones in calcification could provide a better translational outcome for those suffering with cardiovascular calcification.

scholarly journals Vasodilators, Enhancers of Prevention through Exercise of COVID-19?

2020 ◽  
pp. 126-131
Author(s):  
Bogdan- Alexandru Hagiu
Keyword(s):  
Cardiovascular Disease ◽  
Virus Infection ◽  
Angiotensin Converting Enzyme ◽  
Disease Progression ◽  
Mitochondrial Biogenesis ◽  
Future Research ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Over Expression

The role of the angiotensin-converting enzyme 2 (ACE2) receptor in SARS-CoV-2 virus infection and disease progression is complex, and the interaction with exercise is being investigated. However, the virus binds to ACE2. The paper hypothesizes that exceeding the lactic threshold during exercise would cause, through hypoxia, over expression of ACE2. Vasodilators would prevent hypoxia and implicitly this fact. To the complexity of the phenomenon is added the possibility of preventing severe forms of COVID-19 through mitochondrial biogenesis induced by exercise. As a result, the paper examines the ability of antihypertensives used in combination with exercise to treat cardiovascular disease to prevent ACE2 over expression and to stimulate mitochondrial biogenesis. Future research is needed, but it is worth mentioning that some such hypertensives have been proposed for the treatment of COVID-19.

Opposite effects of 17-β estradiol and testosterone on mitochondrial biogenesis and adiponectin synthesis in white adipocytes

2014 ◽  
Vol 52 (2) ◽  
pp. 203-214 ◽  
Author(s):  
Gabriela Capllonch-Amer ◽  
Isabel Lladó ◽  
Ana M Proenza ◽  
Francisco J García-Palmer ◽  
Magdalena Gianotti
Keyword(s):  
Sex Hormones ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Dynamics ◽  
Female Rats ◽  
White Adipocytes ◽  
Proliferation And Differentiation ◽  
New Evidence ◽  
Stimulation Of

Sexual dimorphism has been found in both mitochondrial functionality and adiponectin expression in white adipose tissue, with female rats presenting more functional mitochondria than males and greater adiponectin expression. However, little is known about the role of sex hormones in this dimorphism. The aim was to elucidate the role of sex hormones in mitochondrial biogenesis and dynamics and in adiponectin synthesis in white adipocytes, and also to provide new evidence of the link between these processes. 3T3-L1 preadipocytes were differentiated and treated either with 17-β estradiol (E2; 10 nM), progesterone (Pg), testosterone (1 μM both), or a combination of Pg or testosterone with flutamide (FLT; 10 μM) or E2(1 μM). The markers of mitochondrial biogenesis and dynamics and adiponectin expression were analyzed. E2induced mitochondrial proliferation and differentiation in 3T3-L1, although testosterone showed opposite effects. Pg treatment stimulated proliferation but impaired differentiation. In concerns mitochondrial dynamics, these hormones promoted fusion over fission. FLT treatment indicated that Pg elicits its effects on mitochondrial dynamics through the androgen receptor. E2coadministration with testosterone or Pg reversed its effects. In conclusion, our results show that E2induces stimulation of mitochondrial biogenesis in white adipocytesin vitro, especially in situations that imply an impairment of mitochondrial function, whereas testosterone would have opposite effects. Moreover, testosterone and Pg alter mitochondrial dynamics by promoting fusion over fission, while E2stimulates both processes. All these alterations run in parallel with changes in adiponectin expression, thus suggesting the existence of a link between mitochondrial biogenesis and dynamics and adiponectin synthesis in white adipocytes.

scholarly journals Role of Sex Hormones at Different Physiobiological Conditions and Therapeutic Potential in MBD2 Mediated Severe Asthma

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Binaya Wasti ◽  
Zhifeng Chen ◽  
Yi Ke ◽  
Wen Tao Duan ◽  
Shao-Kun Liu ◽  
...  
Keyword(s):  
Severe Asthma ◽  
Sex Hormones ◽  
Human Body ◽  
Therapeutic Potential ◽  
Corticosteroid Treatment ◽  
Sex Hormone ◽  
Asthma Prevalence ◽  
Term Survival

Sex hormone has become a “hot topic” to evaluate the hormonal therapeutic potential in severe asthma. Th17 cell is one of the main influencing factors involved in the pathogenesis of severe asthma, hence also called as kernel of severe asthma, and Th17 subtype of non-T2 asthma is less responsive (resistance) to inhaled corticosteroid (ICS), so severe in nature. Methyl-CpG binding domain protein 2 (MBD2) is overexpressed and regulates the Th17 differentiation, showing the possibility of therapeutic target in treating Th17 mediated severe asthma. Sex hormone fluctuates at the different physiobiological conditions of the human body and affects the asthma pathobiology showing its role in asthma prevalence, severity, remission, and therapy. This review briefly overviews the sex hormones, their influence in asthma at the different physiobiological conditions of human body, and MBD2 severe asthma connection with the possible therapeutic potential of sex steroids in MBD2 mediated Th17 predominant severe asthma. Male sex hormone tends to show a beneficial effect and possibly downregulates the expression of Th17 cells via regulating MBD2 through a mechanism distinct from corticosteroid treatment and guides us towards discovery of new therapeutic agent, reduces the asthma-related complications, and promotes long-term survival by lowering the risk of therapy-resistant issues of old age severe asthma.

Progress in solving the sex hormone paradox in pulmonary hypertension

2014 ◽  
Vol 307 (1) ◽  
pp. L7-L26 ◽  
Author(s):  
Tim Lahm ◽  
Rubin M. Tuder ◽  
Irina Petrache
Keyword(s):  
Animal Models ◽  
Sex Hormones ◽  
Sex Hormone ◽  
Future Research ◽  
Estrogen Metabolism ◽  
Hormone Synthesis ◽  
17Β Estradiol ◽  
Pulmonary Arterial ◽  
And Gender ◽  
Underlying Mechanisms

Pulmonary arterial hypertension (PAH) is a devastating and progressive disease with marked morbidity and mortality. Even though being female represents one of the most powerful risk factors for PAH, multiple questions about the underlying mechanisms remain, and two “estrogen paradoxes” in PAH exist. First, it is puzzling why estrogens have been found to be protective in various animal models of PAH, whereas PAH registries uniformly demonstrate a female susceptibility to the disease. Second, despite the pronounced tendency for the disease to develop in women, female PAH patients exhibit better survival than men. Recent mechanistic studies in classical and in novel animal models of PAH, as well as recent studies in PAH patients, have significantly advanced the field. In particular, it is now accepted that estrogen metabolism and receptor signaling, as well as estrogen interactions with key pathways in PAH development, appear to be potent disease modifiers. A better understanding of these interactions may lead to novel PAH therapies. It is the purpose of this review to 1) review sex hormone synthesis, metabolism, and receptor physiology; 2) assess the context in which sex hormones affect PAH pathogenesis; 3) provide a potential explanation for the observed estrogen paradoxes and gender differences in PAH; and 4) identify knowledge gaps and future research opportunities. Because the majority of published studies investigated 17β-estradiol and/or its metabolites, this review will primarily focus on pulmonary vascular and right ventricular effects of estrogens. Data for other sex hormones will be discussed very briefly.

scholarly journals The Role of Sex Hormones in Multiple Sclerosis

2018 ◽  
Vol 80 (1-2) ◽  
pp. 93-99 ◽  
Author(s):  
Mirla Avila ◽  
Arpana Bansal ◽  
John Culberson ◽  
Alan N. Peiris
Keyword(s):  
Multiple Sclerosis ◽  
Sex Hormones ◽  
Treatment Strategies ◽  
Female Gender ◽  
Current Treatment ◽  
Sex Hormone ◽  
Immune Mediated ◽  
Autoimmune Conditions ◽  
The Central Nervous System

Multiple sclerosis (MS) is a chronic inflammatory demyelination disorder with an immune-mediated pathophysiology that affects the central nervous system (CNS). Like other autoimmune conditions, it has a predilection for female gender. This suggests a gender bias and a possible hormonal association. Inflammation and demyelination are hallmarks of MS. Oligodendrocytes are the myelinating cells of the CNS and these continue to be generated by oligodendrocyte precursor cells (OPCs). The process of remyelination represents a major form of plasticity in the developing adult CNS. Remyelination does occur in MS, but the process is largely inadequate and/or incomplete. Current treatment strategies primarily focus on reducing inflammation or immunosuppression, but there is a need for more extensive research on re-myelination as a possible mechanism of treatment. Previous studies have shown that pregnancy leads to an increase in OPC proliferation, oligodendrocyte generation and the number of myelinated axons in the maternal CNS. Studies have also suggested that this remyelination is possibly mediated by estriol. Sex hormones in particular have been shown to have an immuno-protective effect in TH1-driven autoimmunity diseases. The aim of our article is to review the available research on sex hormone-specific immune modulatory effects, assess its remyelination potential in MS, and suggest a future path for more extensive research on sex hormone as a target for therapeutics in MS.

scholarly journals Endogenous Sex Hormones and Cardiovascular Disease in Men

2003 ◽  
Vol 88 (11) ◽  
pp. 5076-5086 ◽  
Author(s):  
Majon Muller ◽  
Yvonne T. van der Schouw ◽  
Jos H. H. Thijssen ◽  
Diederick E. Grobbee
Keyword(s):  
Cardiovascular Disease ◽  
Beneficial Effect ◽  
Sex Hormones ◽  
Sex Hormone ◽  
Hormone Production ◽  
Adrenal Androgens ◽  
Prevention And Treatment ◽  
The Relationship ◽  
Circulating Levels ◽  
Endogenous Sex Hormones

Abstract Unlike women, men do not experience an abrupt reduction in endogenous sex hormone production. It has, however, become clear that an age-associated decrease in the levels of (bioactive) sex hormones does occur. Whether endogenous sex hormones have an impact on cardiovascular disease has for many years remained largely unknown, but during the last decade more attention has been drawn to the importance of testosterone, estrogens, and adrenal androgens in etiology, prevention, and treatment of male cardiovascular disease. The purpose of this article is to summarize the evidence currently available on the association between endogenous sex hormones and cardiovascular disease in males. Published studies dealing with the relationship between circulating levels of sex hormones and cardiovascular disease in males were reviewed. The studies reviewed in this article suggest that circulating endogenous sex hormones and estrogens have a neutral or beneficial effect on cardiovascular disease in men.

scholarly journals Hyperglycemia decreases mitochondrial function: The regulatory role of mitochondrial biogenesis

2007 ◽  
Vol 225 (2) ◽  
pp. 214-220 ◽  
Author(s):  
Carlos M. Palmeira ◽  
Anabela P. Rolo ◽  
Jessica Berthiaume ◽  
James A. Bjork ◽  
Kendall B. Wallace
Keyword(s):  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Regulatory Role

scholarly journals Post-Transplant Cardiovascular Disease

2021 ◽  
pp. CJN.00520121
Author(s):  
Kelly A. Birdwell ◽  
Meyeon Park
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Kidney Transplant ◽  
Optimal Strategies ◽  
Future Research ◽  
Kidney Transplant Recipients ◽  
Post Transplant ◽  
Treatment And Prevention ◽  
Artery Disease

Cardiovascular disease remains a leading cause of death and morbidity in kidney transplant recipients and a common reason for post-transplant hospitalization. Several traditional and nontraditional cardiovascular risk factors exist, and many of them present pretransplant and worsened, in part, due to the addition of immunosuppression post-transplant. We discuss optimal strategies for identification and treatment of these risk factors, including the emerging role of sodium-glucose cotransporter 2 inhibitors in post-transplant diabetes and cardiovascular disease. We present common types of cardiovascular disease observed after kidney transplant, including coronary artery disease, heart failure, pulmonary hypertension, arrhythmia, and valvular disease. We also discuss screening, treatment, and prevention of post-transplant cardiac disease. We highlight areas of future research, including the need for goals and best medications for risk factors, the role of biomarkers, and the role of screening and intervention.

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