Estrogen-induced cardiorenal protection: potential cellular, biochemical, and molecular mechanisms

2001 ◽  
Vol 280 (3) ◽  
pp. F365-F388 ◽  
Author(s):  
Raghvendra K. Dubey ◽  
Edwin K. Jackson
Keyword(s):  
Estrogen Receptor ◽  
Vascular Remodeling ◽  
Molecular Mechanisms ◽  
Vascular Wall ◽  
Protective Effects ◽  
Vascular Disorders ◽  
Biochemical Processes ◽  
Cardiovascular Systems ◽  
Protection Potential

A number of cellular and biochemical processes are involved in the pathophysiology of glomerular and vascular remodeling, leading to renal and vascular disorders, respectively. Although estradiol protects the renal and cardiovascular systems, the mechanisms involved remain unclear. In this review we provide a discussion of the cellular, biochemical, and molecular mechanisms by which estradiol may exert protective effects on the kidneys and vascular wall. In this regard, we consider the possible role of genomic vs. nongenomic mechanisms and estrogen receptor-dependent vs. estrogen receptor-independent mechanisms in mediating the protective effects of estradiol on the renal and cardiovascular systems.

scholarly journals Estrogen Receptor and Vascular Aging

2021 ◽  
Vol 2 ◽  
Author(s):  
Morgane Davezac ◽  
Melissa Buscato ◽  
Rana Zahreddine ◽  
Patrick Lacolley ◽  
Daniel Henrion ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Cardiovascular Diseases ◽  
Experimental Studies ◽  
Hormonal Treatment ◽  
Protective Effects ◽  
Age Related ◽  
Nuclear Receptor Family ◽  
The Impact ◽  
Receptor Family

Cardiovascular diseases remain an age-related pathology in both men and women. These pathologies are 3-fold more frequent in men than in women before menopause, although this difference progressively decreases after menopause. The vasculoprotective role of estrogens are well established before menopause, but the consequences of their abrupt decline on the cardiovascular risk at menopause remain debated. In this review, we will attempt to summarize the main clinical and experimental studies reporting the protective effects of estrogens against cardiovascular diseases, with a particular focus on atherosclerosis, and the impact of aging and estrogen deprivation on their endothelial actions. The arterial actions of estrogens, but also part of that of androgens through their aromatization into estrogens, are mediated by the estrogen receptor (ER)α and ERβ. ERs belong to the nuclear receptor family and act by transcriptional regulation in the nucleus, but also exert non-genomic/extranuclear actions. Beside the decline of estrogens at menopause, abnormalities in the expression and/or function of ERs in the tissues, and particularly in arteries, could contribute to the failure of classic estrogens to protect arteries during aging. Finally, we will discuss how recent insights in the mechanisms of action of ERα could contribute to optimize the hormonal treatment of the menopause.

CALCIUM AND VITAMIN : EFFECTS ON BONE TISSUE AND VASCULAR REMODELING (LITERATURE REVIEW)

2021 ◽  
pp. 1200-1208
Author(s):  
С. В. Булгакова ◽  
Е. В. Тренева ◽  
Н. О. Захарова ◽  
А. В. Николаева
Keyword(s):  
Literature Review ◽  
Vascular Remodeling ◽  
Molecular Mechanisms ◽  
Vascular Wall ◽  
Arterial Calcification ◽  
Mineral Density ◽  
Treatment And Prevention ◽  
Calcium Deposits ◽  
Local Accumulation ◽  
Progression Of Atherosclerosis

Препараты кальция входят в схемы лечения и профилактики низкой минеральной плотности костной ткани. Однако последние научные исследования показали, что дополнительное поступление кальция может увеличить риск сердечно-сосудистых заболеваний. Это связано с отложением кальция в эндотелии кровеносных сосудов. Значимость минерализации сосудистой стенки не ограничивается локальным накоплением кальциевых депозитов, но в значительной мере определяется их активирующим влиянием на прогрессирование атеросклероза. Витамин К играет важную роль в гомеостазе кальция, снижает артериальную кальцификацию и артериальную жесткость и, как следствие, оказывает протективный эффект при приеме кальция. В данном обзоре литературы представлена современная информация о кальциевом парадоксе, обсуждаются основные молекулярные механизмы кальцификации сосудов, рассмотрены терапевтические стратегии лечения витамином К . Calcium preparations are included in the treatment and prevention regimens for low bone mineral density. However, recent scientific studies have shown that additional calcium intake can increase the risk of heart disease, which is associated with the deposition of calcium in the endothelium of blood vessels. The significance of vascular wall mineralization is not limited to local accumulation of calcium deposits, but is largely determined by their activating effect on the progression of atherosclerosis. Vitamin K plays an important role in calcium homeostasis, reduces arterial calcification and arterial stiffness and, as a result, has a protective effect when taking calcium. This literature review provides current information about the calcium paradox, discusses the main molecular mechanisms of vascular calcification, and considers therapeutic strategies for vitamin К treatment.

scholarly journals Molecular mechanisms of estrogen receptor β-induced apoptosis and autophagy in tumors: implication for treating osteosarcoma

2019 ◽  
Vol 47 (10) ◽  
pp. 4644-4655
Author(s):  
Zheng-ming Yang ◽  
Min-fei Yang ◽  
Wei Yu ◽  
Hui-min Tao
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptors ◽  
Tumor Cells ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Critical Role ◽  
Osteosarcoma Cells ◽  
Proliferation And Metastasis ◽  
Induced Apoptosis

The estrogen receptors α (ERα) and β (ERβ) are located in the nucleus and bind to estrogen to initiate transcription of estrogen-responsive genes. In a variety of tumor cells, ERβ has been shown to be a tumor suppressor. In particular, ERβ has anti-proliferative effects in osteosarcoma cells. Additionally, ERβ has been proven to regulate the apoptosis-related molecules IAP, BAX, caspase-3, and PARP, and to act on the NF-κB/BCL-2 pathway to induce apoptosis in tumors. Moreover, ERβ can regulate the expression of the autophagy associated markers LC3-I/LC-3II and p62 and induce autophagy in tumors by inhibiting the PI3K/AKT/mTOR pathway and activating the AMPK pathway. Here, we review the molecular mechanisms by which ERβ induces apoptosis and autophagy in a variety of tumors to further delineate more specific molecular mechanisms underlying osteosarcoma tumorigenesis and pathogenesis. Considering the broad involvement of ERβ in apoptosis, autophagy, and their interaction, it is plausible that the critical role of ERβ in inhibiting the proliferation and metastasis of osteosarcoma cells is closely related to its regulation of apoptosis and autophagy.

scholarly journals Niacin Attenuates Pulmonary Hypertension Through H-PGDS in Macrophages

2020 ◽  
Vol 127 (10) ◽  
pp. 1323-1336
Author(s):  
Daile Jia ◽  
Peiyuan Bai ◽  
Naifu Wan ◽  
Jiao Liu ◽  
Qian Zhu ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Vascular Remodeling ◽  
Molecular Mechanisms ◽  
Growth Factor Receptor ◽  
Lipid Lowering ◽  
Hypoxic Exposure ◽  
Protective Effects ◽  
Perivascular Inflammation ◽  
Lowering Drug ◽  
Endothelial Growth Factor

Rationale: Pulmonary arterial hypertension (PAH) is characterized by progressive pulmonary vascular remodeling, accompanied by varying degrees of perivascular inflammation. Niacin, a commonly used lipid-lowering drug, possesses vasodilating and proresolution effects by promoting the release of prostaglandin D 2 (PGD 2 ). However, whether or not niacin confers protection against PAH pathogenesis is still unknown. Objective: This study aimed to determine whether or not niacin attenuates the development of PAH and, if so, to elucidate the molecular mechanisms underlying its effects. Methods and Results: Vascular endothelial growth factor receptor inhibitor SU5416 and hypoxic exposure were used to induce pulmonary hypertension (PH) in rodents. We found that niacin attenuated the development of this hypoxia/SU5416–induced PH in mice and suppressed progression of monocrotaline-induced and hypoxia/SU5416–induced PH in rats through the reduction of pulmonary artery remodeling. Niacin boosted PGD 2 generation in lung tissue, mainly through H-PGDS (hematopoietic PGD 2 synthases). Deletion of H-PGDS, but not lipocalin-type PGDS, exacerbated the hypoxia/SU5416–induced PH in mice and abolished the protective effects of niacin against PAH. Moreover, H-PGDS was expressed dominantly in infiltrated macrophages in lungs of PH mice and patients with idiopathic PAH. Macrophage-specific deletion of H-PGDS markedly decreased PGD 2 generation in lungs, aggravated hypoxia/SU5416–induced PH in mice, and attenuated the therapeutic effect of niacin on PAH. Conclusions: Niacin treatment ameliorates the progression of PAH through the suppression of vascular remodeling by stimulating H-PGDS–derived PGD 2 release from macrophages.

scholarly journals A Role of Ginseng and Its Constituents in the Treatment of Central Nervous System Disorders

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Natasya Trivena Rokot ◽  
Timothy Sean Kairupan ◽  
Kai-Chun Cheng ◽  
Joshua Runtuwene ◽  
Nova Hellen Kapantow ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Molecular Mechanisms ◽  
Protective Effects ◽  
Pharmacological Effects ◽  
Intestinal Metabolism ◽  
Traditional Herbal Medicine ◽  
Perennial Plant ◽  
Enhanced Properties

Ginseng, a perennial plant belonging to thePanaxgenus of the Araliaceae family, has been used in China, Korea, and Japan as a traditional herbal medicine for thousands of years. Ginseng is recorded to have exhibited a wide variety of beneficial pharmacological effects and has become a popular and worldwide known health supplement and drug. The protective effects of ginseng on central nervous system are discussed in this review. Ginseng species and ginsenosides and their intestinal metabolism and bioavailability are concisely introduced. The molecular mechanisms of the effects of ginseng on central nervous system, mainly focused on the neuroprotection properties of ginseng, memory, and learning enhanced properties, and the effects on neurodegenerative disorders are presented. Thus, ginseng and its constituents are of potential merits in the treatment of cerebral disorders.

scholarly journals The Potential of Hydrogen Sulfide Donors in Treating Cardiovascular Diseases

2021 ◽  
Vol 22 (4) ◽  
pp. 2194
Author(s):  
Yi-Zhen Wang ◽  
Ebenezeri Erasto Ngowi ◽  
Di Wang ◽  
Hui-Wen Qi ◽  
Mi-Rong Jing ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Cardiovascular Diseases ◽  
Molecular Mechanisms ◽  
Heart Function ◽  
Cell Types ◽  
Special Focus ◽  
Protective Effects ◽  
Improve Heart Function ◽  
Different Cell Types

Hydrogen sulfide (H2S) has long been considered as a toxic gas, but as research progressed, the idea has been updated and it has now been shown to have potent protective effects at reasonable concentrations. H2S is an endogenous gas signaling molecule in mammals and is produced by specific enzymes in different cell types. An increasing number of studies indicate that H2S plays an important role in cardiovascular homeostasis, and in most cases, H2S has been reported to be downregulated in cardiovascular diseases (CVDs). Similarly, in preclinical studies, H2S has been shown to prevent CVDs and improve heart function after heart failure. Recently, many H2S donors have been synthesized and tested in cellular and animal models. Moreover, numerous molecular mechanisms have been proposed to demonstrate the effects of these donors. In this review, we will provide an update on the role of H2S in cardiovascular activities and its involvement in pathological states, with a special focus on the roles of exogenous H2S in cardiac protection.

scholarly journals Molecular Mechanisms of Adiponectin-Induced Attenuation of Mechanical Stretch-Mediated Vascular Remodeling

2020 ◽  
Vol 2020 ◽  
pp. 1-15 ◽  
Author(s):  
Crystal M. Ghantous ◽  
Rima Farhat ◽  
Laiche Djouhri ◽  
Sarah Alashmar ◽  
Gulsen Anlar ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Vascular Remodeling ◽  
Molecular Mechanisms ◽  
Nuclear Translocation ◽  
Mechanical Stretch ◽  
Leucine Incorporation ◽  
Ros Generation ◽  
Dependent Manner ◽  
Protective Effects ◽  
Vascular Hypertrophy

Hypertension induces vascular hypertrophy, which changes blood vessels structurally and functionally, leading to reduced tissue perfusion and further hypertension. It is also associated with dysregulated levels of the circulating adipokines leptin and adiponectin (APN). Leptin is an obesity-associated hormone that promotes vascular smooth muscle cell (VSMC) hypertrophy. APN is a cardioprotective hormone that has been shown to attenuate hypertrophic cardiomyopathy. In this study, we investigated the molecular mechanisms of hypertension-induced VSMC remodeling and the involvement of leptin and APN in this process. To mimic hypertension, the rat portal vein (RPV) was mechanically stretched, and the protective effects of APN on mechanical stretch-induced vascular remodeling and the molecular mechanisms involved were examined by using 10 μg/ml APN. Mechanically stretching the RPV significantly decreased APN protein expression after 24 hours and APN mRNA expression in a time-dependent manner in VSMCs. The mRNA expression of the APN receptors AdipoR1, AdipoR2, and T-cadherin significantly increased after 15 hours of stretch. The ratio of APN/leptin expression in VSMCs significantly decreased after 24 hours of mechanical stretch. Stretching the RPV for 3 days increased the weight and [3H]-leucine incorporation significantly, whereas APN significantly reduced hypertrophy in mechanically stretched vessels. Stretching the RPV for 10 minutes significantly decreased phosphorylation of LKB1, AMPK, and eNOS, while APN significantly increased p-LKB1, p-AMPK, and p-eNOS in stretched vessels. Mechanical stretch significantly increased p-ERK1/2 after 10 minutes, whereas APN significantly reduced stretch-induced ERK1/2 phosphorylation. Stretching the RPV also significantly increased ROS generation after 1 hour, whereas APN significantly decreased mechanical stretch-induced ROS production. Exogenous leptin (3.1 nM) markedly increased GATA-4 nuclear translocation in VSMCs, whereas APN significantly attenuated leptin-induced GATA-4 nuclear translocation. Our results decipher molecular mechanisms of APN-induced attenuation of mechanical stretch-mediated vascular hypertrophy, with the promising potential of ultimately translating this protective hormone into the clinic.

scholarly journals ADAMTS Proteins and Vascular Remodeling in Aortic Aneurysms

Biomolecules ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 12
Author(s):  
Zakaria Mougin ◽  
Julia Huguet Herrero ◽  
Catherine Boileau ◽  
Carine Le Goff
Keyword(s):  
Vascular Remodeling ◽  
Potential Role ◽  
Dynamic Structure ◽  
Vascular Wall ◽  
Aortic Aneurysms ◽  
Cellular Behavior ◽  
Thoracic Aortic Aneurysms ◽  
Abdominal Aortic ◽  
Different Types

Extracellular matrix (ECM) in the vascular wall is a highly dynamic structure composed of a set of different molecules such as elastins, collagens, fibronectin (Fn), laminins, proteoglycans, and polysaccharides. ECM undergoes remodeling processes to regulate vascular smooth muscle and endothelial cells’ proliferation, differentiation, and adhesion. Abnormalities affecting the ECM can lead to alteration in cellular behavior and from this, this can conduce to the development of pathologies. Metalloproteases play a key role in maintaining the homeostasis of ECM by mediating the cleavage of different ECM components. There are different types of metalloproteases: matrix metalloproteinases (MMPs), disintegrin and metalloproteinases (ADAMs), and ADAMs with thrombospondin motifs (ADAMTSs). ADAMTSs have been found to participate in cardiovascular physiology and diseases and specifically in aortic aneurysms. This review aims to decipher the potential role of ADAMTS proteins in the physiopathologic development of Thoracic Aortic Aneurysms (TAA) and Abdominal Aortic Aneurysms (AAA). This review will focus on what is known on the ADAMTS family involved in human aneurysms from human tissues to mouse models. The recent findings on THSD4 (encoding ADAMTSL6) mutations in TAA give a new insight on the involvement of the ADAMTS family in TAA.

scholarly journals THE ROLE OF VASCULAR REMODELING IN THE FORMATION OF STRUCTURAL PHENOTYPES OF OSTEOARTHRITIS

2018 ◽  
Vol 25 (3) ◽  
pp. 61-67
Author(s):  
M. A. KABALYK ◽  
V. A. NEVZOROVA
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Knee Joint ◽  
Vascular Remodeling ◽  
Structural Changes ◽  
Vascular Wall ◽  
External Diameter ◽  
Resonance Imaging ◽  
Structural Progression

Aim. Evaluation of the role of vascular remodeling in the formation of structural phenotypes of osteoarthritis (OA).Materials and methods. 62 patients with OA aged 65,9±8,8 years and 18 volunteers without clinical and roentgenologic signs of OA aged 60,7±7,9 years were examined. All patients underwent magnetic resonance imaging of knee joints. To analyze the structural changes in the tissues of the knee joint, the WORMS protocol was used for magnetic resonance imaging. The thickness of the vascular wall, the external diameter, the vascular index (VI) were measured – the ratio of the diameter of the lumen of the vessel to the thickness of the popliteal artery (PA) wall, the branch of the upper lateral artery (LA), the medial artery of the knee (MA).Results. The analysis of the parameters of the arteries of the knee joint showed that with a subchondral OA phenotype, the thickness of the PA wall is statistically significantly larger than the cartilage phenotype, and the vascular index of the PA is significantly higher in the group of the cartilaginous phenotype. The upper LA wall was significantly thicker in the subchondral OA phenotype. VI of the upper LA was significantly lower in patients with a subchondral phenotype compared with the cartilaginous phenotype. The thickness of the MA wall was also larger with a bone phenotype, and VI with a cartilaginous phenotype.Conclusion. The results of the study showed the relationship between vascular remodeling and structural progression of OA. Changes in the vascular wall adversely affect all joint tissues, leading to their remodeling. It was established that the degree of vascular remodeling determines the formation of structural OA phenotypes. Severe vascular changes are associated with the subchondral OA phenotype.

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