Circulating microparticles as indicators of cardiometabolic risk in PCOS

Yalameha, Banafsheh; Nejabati, Hamid Reza; Nouri, Mohammad

doi:10.1016/j.cca.2022.06.019

Cited by 4 publications

(5 citation statements)

References 119 publications

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“…The conditions mentioned above involve complex genetic and environmental interplays, rendering them less amenable to gene therapy (201). Attaining consistent (184). The intramyocardial injection of adenoviral VEGF was safe and improved myocardial perfusion at 1 year in patients with severe CAD, as shown in phase I/II experiment.…”

Section: Gene Therapymentioning

confidence: 93%

“…Platelet-derived microparticles (PMPs) have been demonstrated to play a role in the increased incidence of atherosclerotic plaque and arterial thrombosis formation in individuals ( 182 , 183 ). It is indisputable that patients with CVD exhibit platelets with a hyperactive phenotype characterized by higher aggregation, activation, and adhesion ( 184 ). This may contribute to the emergence of atherothrombotic complications in such patients ( 185 ).…”

Section: Role Of Mets On Platelet Hyperactivitymentioning

confidence: 99%

“…However, two additional benefits of improved redox balance are lowered NOX activity and eNOS coupling. VEGF may also stimulate NRF-2-mediated antioxidant mechanisms ( 184 ). The intramyocardial injection of adenoviral VEGF was safe and improved myocardial perfusion at 1 year in patients with severe CAD, as shown in phase I/II experiment.…”

Section: Advanced/alternative Treatment Strategiesmentioning

confidence: 99%

“…Modifying one’s lifestyle, especially diet, is the most important therapeutic strategy for this condition. Certain dietary modifications have been demonstrated to effectively reduce symptoms and improve several metrics associated with MetS ( 184 ). Scientific studies showed that the DASH (Dietary Approaches to Stop Hypertension) diet is the most effective strategy for preventing and treating MetS compared to low-fat and restricted diets.…”

Section: Advanced/alternative Treatment Strategiesmentioning

confidence: 99%

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Endothelial dysfunction, platelet hyperactivity, hypertension, and the metabolic syndrome: molecular insights and combating strategies

Das

Banerjee

et al. 2023

Front. Nutr.

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Metabolic syndrome (MetS) is a multifaceted condition that increases the possibility of developing atherosclerotic cardiovascular disease. MetS includes obesity, hypertension, dyslipidemia, hyperglycemia, endothelial dysfunction, and platelet hyperactivity. There is a concerning rise in the occurrence and frequency of MetS globally. The rising incidence and severity of MetS need a proactive, multipronged strategy for identifying and treating those affected. For many MetS patients, achieving recommended goals for healthy fat intake, blood pressure control, and blood glucose management may require a combination of medicine therapy, lifestyles, nutraceuticals, and others. However, it is essential to note that lifestyle modification should be the first-line therapy for MetS. In addition, MetS requires pharmacological, nutraceutical, or other interventions. This review aimed to bring together the etiology, molecular mechanisms, and dietary strategies to combat hypertension, endothelial dysfunction, and platelet dysfunction in individuals with MetS.

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Section: Gene Therapymentioning

confidence: 93%

Section: Role Of Mets On Platelet Hyperactivitymentioning

confidence: 99%

Section: Advanced/alternative Treatment Strategiesmentioning

confidence: 99%

Section: Advanced/alternative Treatment Strategiesmentioning

confidence: 99%

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Endothelial dysfunction, platelet hyperactivity, hypertension, and the metabolic syndrome: molecular insights and combating strategies

Das

Banerjee

et al. 2023

Front. Nutr.

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“…Polycystic ovary syndrome (PCOS) is a reproductive endocrine disorder that affects 5%–18% of women of childbearing age worldwide [ 1 ]. The clinical manifestations of PCOS include hyperandrogenism and oligoovulation, which are generally accompanied by metabolic abnormalities such as insulin resistance (IR), obesity, and cardiovascular diseases [ 2 – 4 ]. Nevertheless, owing to the heterogeneity of the condition and the absence of a well-defined pathogenic mechanism, at present, research and treatment achievements for PCOS are relatively limited.…”

Section: Introductionmentioning

confidence: 99%

BOP1 contributes to the activation of autophagy in polycystic ovary syndrome via nucleolar stress response

Ji,

Zhang,

Yang

et al. 2024

Cell. Mol. Life Sci.

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Abnormal autophagy is one of the vital features in polycystic ovary syndrome (PCOS). However, the underlying molecular mechanisms remain unelucidated. In this study, we aimed to investigate whether Block of Proliferation 1 (BOP1) is involved in the onset of autophagy activation of granulosa cells in PCOS. Firstly, we found that BOP1 expression was significantly down-regulated in the ovaries of PCOS mice, which was associated with the development of PCOS. Next, local injection of lentiviral vectors in the ovary for the overexpression of BOP1 significantly alleviated the phenotypes of elevated androgens, disturbed estrous cycle, and abnormal follicular development in PCOS mice. Subsequently, we found that knockdown of BOP1 activated autophagy of granulosa cells in the in vitro experiments, whereas overexpression of BOP1 inhibited autophagy in both in vivo and in vitro models. Mechanistically, BOP1 knockdown triggered the nucleolus stress response, which caused RPL11 to be released from the nucleolus into the nucleoplasm and inhibited the E3 ubiquitination ligase of MDM2, thereby enhancing the stability of p53. Subsequently, P53 inhibited mTOR, thereby activating autophagy in granulosa cells. In addition, the mRNA level of BOP1 was negatively correlated with antral follicle count (AFC), body–mass index (BMI), serum androgen levels, and anti-Mullerian hormone (AMH) in patients with PCOS. In summary, our study demonstrates that BOP1 downregulation inhibits mTOR phosphorylation through activation of the p53-dependent nucleolus stress response, which subsequently contributes to aberrant autophagy in granulosa cells, revealing that BOP1 may be a key target for probing the mechanisms of PCOS.

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Extracellular Vesicles in Thalassemia: Mechanisms, Implications, and Therapeutic Potential

Jiskani

2024

Aspects of Molecular Medicine

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Circulating microparticles as indicators of cardiometabolic risk in PCOS

Cited by 4 publications

References 119 publications

Endothelial dysfunction, platelet hyperactivity, hypertension, and the metabolic syndrome: molecular insights and combating strategies

Endothelial dysfunction, platelet hyperactivity, hypertension, and the metabolic syndrome: molecular insights and combating strategies

BOP1 contributes to the activation of autophagy in polycystic ovary syndrome via nucleolar stress response

Extracellular Vesicles in Thalassemia: Mechanisms, Implications, and Therapeutic Potential

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