Angiopoietin‐2 regulates the phenotypic switch of vascular smooth muscle cells DOI

Xiaowen Gan,

Shenjiao Lu,

Fen Ning

и другие.

The FASEB Journal, Год журнала: 2025, Номер 39(5)

Опубликована: Март 3, 2025

Abstract During uterine spiral artery remodeling, vascular smooth muscle cells (VSMCs) become disorganized and undergo phenotypic switching from a contractile to more synthetic phenotype. We have previously reported that natural killer induce this VSMC by secreting angiopoietin‐2 (Ang‐2). Here, we identified the specific mechanisms which Ang‐2 plays role in phenomenon. VSMCs isolated human umbilical arteries were used as an vitro model investigate of switching. Human decidua tissue preeclamptic control pregnancies was collected compare expression levels related proteins. induced phenotype evidenced decreased marker expression, increased proliferation migration, altered cytoskeleton. expressed integrin β6 interacted directly with phosphorylation FAK (S910 Y397), AKT (S473), mTOR (S2448). Knockdown recovered calponin loss resulted lower EZH2 abundance. Inhibition both attenuated Ang‐2‐induced inhibition LC3 II/LC3 I ratio ATG7 proliferation. Lipid peroxidation ferrostatin‐1 or IL‐8 receptor antagonist navarixin inhibited migration. secretion significantly lipid inhibition. In decidua, there unremodeled arteries, abundance dysregulated. dysregulation may disrupt remodeling contribute preeclampsia. be novel therapeutic target for treatment pregnancy complications affected incomplete remodeling.

Язык: Английский

Regulated Cell Death in Endometriosis DOI Creative Commons
Erqing Huang,

Xiaoli Wang,

Lijuan Chen

и другие.

Biomolecules, Год журнала: 2024, Номер 14(2), С. 142 - 142

Опубликована: Янв. 23, 2024

Regulated cell death (RCD) represents a distinct mode of demise, differing from accidental (ACD), characterized by specific signaling cascades orchestrated diverse biomolecules. The regular process plays crucial role in upholding internal homeostasis, acting as safeguard against biological or chemical damage. Nonetheless, programmed deaths have the potential to activate an immune–inflammatory response, potentially contributing diseases enlisting immune cells and releasing pro-inflammatory factors. Endometriosis, prevalent gynecological ailment, remains incompletely understood despite substantial progress unraveling associated pathways. Its complexity is intricately tied dysregulation inflammatory responses, with various RCD processes such apoptosis, autophagic death, pyroptosis, ferroptosis implicated its development. Notably, limited research explores association between endometriosis pathways like pyroptosis cuproptosis. exploration regulated context holds tremendous for further advancements. This article thoroughly reviews molecular mechanisms governed their implications endometriosis. A comprehensive understanding mechanism has catalyze development promising therapeutic strategies chart course future directions field.

Язык: Английский

Процитировано

7

Oxidative Imbalance in Endometriosis-Related Infertility—The Therapeutic Role of Antioxidants DOI Open Access
Izabela Dymanowska-Dyjak, Karolina Frankowska, Monika Abramiuk

и другие.

International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(12), С. 6298 - 6298

Опубликована: Июнь 7, 2024

Endometriosis in half of affected women is closely related to problems with fertility. Endometriosis-associated infertility caused by a wide range abnormalities affecting the female reproductive tract, from oocyte quality impairment disturbances eutopic endometrium or mechanical resulting disease progression. Since supportive antioxidant therapies, addition surgical treatment assisted techniques (ARTs), have overall been proven be effective tools endometriosis management, objective our review was analyze role substances, including vitamins, micronutrients, N-acetylcysteine (NAC), curcumin, melatonin, and resveratrol, endometriosis-related infertility. Most these substances alleviate systemic oxidant predominance, which has expressed through decreased oxidative stress (OS) markers enhanced antioxidative defense. In addition, we demonstrated that predominant effect aforementioned inhibition development endometriotic lesions as well suppression pro-inflammatory molecules. Although can undoubtedly conclude antioxidants are beneficial fertility support, further studies explaining detailed pathways their action needed.

Язык: Английский

Процитировано

7

Ferroptosis and oxidative stress in endometriosis: A systematic review of the literature DOI Creative Commons
Chenghong Ni, Dingheng Li

Medicine, Год журнала: 2024, Номер 103(11), С. e37421 - e37421

Опубликована: Март 15, 2024

Endometriosis (EMT) a common gynecological condition in women, an inflammatory disease characterized by the presence of endometrial tissue on organs and tissues pelvis, is mainly associated with chronic pelvic pain infertility. As etiology has not been fully elucidated, current treatment limited to surgery, hormones painkillers, more side effects difficulty achieving long-term relief. Oxidative stress manifests itself as overproduction reactive oxygen species, which integral impact pathology female reproductive disorders. In this review, we evaluate mechanisms iron overload-induced oxidative ferroptosis EMT their pathophysiological implications.

Язык: Английский

Процитировано

6

Ferroptosis induced by iron overload promotes fibrosis in ovarian endometriosis and is related to subpopulations of endometrial stromal cells DOI Creative Commons
Yanqin Zhang, Xinyu Liu, Mengqi Deng

и другие.

Frontiers in Pharmacology, Год журнала: 2022, Номер 13

Опубликована: Сен. 2, 2022

Endometriosis (EMs) is defined as the presence of tissue somewhat resembling endometrial glands and stroma outside uterus; retrograded endometrium grows in peritoneal cavity elicits fibrosis. Ferroptosis a recently discovered form programmed cell death, which iron-dependent. The induction ferroptosis has been found to participate However, relationship between EMs fibrosis remains unknown. In this study, we confirmed that iron content ectopic stromal ovarian significantly increased. We explored role iron-induced pathogenesis for first time. tissues was enhanced than eutopic tissues. Furthermore, performed vivo drug screening induced by ferric ammonium citrate (FAC) could aggravate To clarify mechanism process, composition human uterine characterized. Fibroblast-specific protein-1 used fibroblasts, smooth muscle actin alpha myofibroblasts, platelet-derived growth factor receptor beta (CD140b) mesenchymal cells (MSCs). results demonstrated percentage myofibroblasts higher portion MSCs lower those endometrium. Moreover, proportion decreased increased considerably after FAC treatment vitro. disruption intracellular levels or via chelation deferoxamine mesylate inhibitor ferrostatin-1 reverse indicating plays vital Considering accumulation can feed Fenton reaction generate unquenchable amounts free radicals, causing damage thereby contributing fibrosis, validated underlying excess facilitate fibrotic responses. Collectively, these data provide evidence supernumerary key regulator promoting inducing

Язык: Английский

Процитировано

24

A transcriptomic analysis of the interplay of ferroptosis and immune filtration in endometriosis and identification of novel therapeutic targets DOI
Sonia Chadha

Computational Biology and Chemistry, Год журнала: 2025, Номер 115, С. 108343 - 108343

Опубликована: Янв. 7, 2025

Язык: Английский

Процитировано

0

Ferroptosis in Endometriosis: Traditional Chinese Medicine Interventions and Mechanistic Insights DOI

Dazhi Lan,

Shuping Huang, Jing Li

и другие.

The American Journal of Chinese Medicine, Год журнала: 2025, Номер unknown, С. 1 - 24

Опубликована: Март 27, 2025

Endometriosis (EMS) is a chronic, estrogen-dependent inflammatory disease affecting 5–10% of women reproductive age, characterized by the growth endometrial tissue on outside uterus. The dysregulation iron metabolism leads to accumulation ions at lesion sites, resulting in oxidative stress and pro-inflammatory responses that promote progression EMS. mechanisms underlying ferroptosis EMS primarily involve accumulation, lipid peroxidation, loss glutathione peroxidase 4 activity. These confer resistance within ectopic tissues facilitate cell survival proliferation. Traditional Chinese medicine (TCM) has demonstrated therapeutic potential for modulating ferroptosis. Studies have shown TCM monomers may regulate transport proteins anti-oxidant defense mechanisms. formulas employ distinct treatment strategies depending stage EMS: early stages, they control growth, whereas later inhibit reduce inflammation order improve health slow progression. This study provides new perspective management summarizing role its pathological reviewing findings use regulating

Язык: Английский

Процитировано

0

Modulation of the p38 MAPK Pathway by Anisomycin Promotes Ferroptosis of Hepatocellular Carcinoma through Phosphorylation of H3S10 DOI Creative Commons
Wei Chen, Wenjing Yang, Chunyan Zhang

и другие.

Oxidative Medicine and Cellular Longevity, Год журнала: 2022, Номер 2022, С. 1 - 20

Опубликована: Ноя. 24, 2022

Hepatocellular carcinoma (HCC) is a prevalent malignant tumor worldwide. Ferroptosis emerging as an effective target for treatment it has been shown to potentiate cell death in some malignancies. However, remains unclear whether histone phosphorylation events, epigenetic mechanism that regulates transcriptional expression, are involved ferroptosis. Our study found supplementation with anisomycin, agonist of p38 mitogen-activated protein kinase (MAPK), induced ferroptosis HCC cells, and the H3 on serine 10 (p-H3S10) was participated anisomycin-induced To investigate anticancer effects anisomycin-activated MAPK HCC, we analyzed viability, colony formation, death, migration Hep3B HCCLM3 cells. The results showed anisomycin could significantly suppress formation induce death. hallmarks ferroptosis, such abnormal accumulation iron elevated levels lipid peroxidation malondialdehyde, were detected confirm ability promote Furthermore, coincubation SB203580, inhibitor activated MAPK, partially rescued And p-p38 p-H3S10 successively increased by treatment. relationship between revealed ChIP sequencing. reverse transcription PCR immunofluorescence NCOA4 upregulated both mRNA after C11-BODIPY staining, reactive oxygen species reduced knockdown. In conclusion, promoted cells through H3S10 phosphorylation.

Язык: Английский

Процитировано

20

Current Understanding of and Future Directions for Endometriosis-Related Infertility Research with a Focus on Ferroptosis DOI Creative Commons
Hiroshi Kobayashi,

Chiharu Yoshimoto,

Sho Matsubara

и другие.

Diagnostics, Год журнала: 2023, Номер 13(11), С. 1926 - 1926

Опубликована: Май 31, 2023

To date, the development of therapy for endometriosis and disease-related infertility remains a major challenge. Iron overload caused by periodic bleeding is hallmark endometriosis. Ferroptosis an iron- lipid-reactive oxygen species-dependent type programmed cell death that distinct from apoptosis, necrosis, autophagy. This review summarizes current understanding future directions research treatment infertility, with main focus on molecular basis ferroptosis in endometriotic granulosa cells. Papers published between 2000 2022 PubMed Google Scholar databases were included this review. Emerging evidence suggests closely linked to pathophysiology Endometriotic cells are characterized resistance, whereas remain highly susceptible ferroptosis, suggesting regulation utilized as interventional target into infertility. New therapeutic strategies urgently needed efficiently kill while protecting An analysis pathway vitro, vivo, animal enhances our pathogenesis disease. Here, we discuss role modulators approach potential novel

Язык: Английский

Процитировано

12

Spotlight on iron overload and ferroptosis: Research progress in female infertility DOI
Jinghua Zhang, Tiantian Su, Yuan Fan

и другие.

Life Sciences, Год журнала: 2023, Номер 340, С. 122370 - 122370

Опубликована: Дек. 22, 2023

Язык: Английский

Процитировано

11

Suppressing MTERF3 inhibits proliferation of human hepatocellular carcinoma via ROS-mediated p38 MAPK activation DOI Creative Commons
Zhihai Zheng,

Youjuan Zhao,

Hongjia Yu

и другие.

Communications Biology, Год журнала: 2024, Номер 7(1)

Опубликована: Янв. 5, 2024

Abstract Mitochondrial transcription termination factor 3 (MTERF3) negatively regulates mitochondrial DNA transcription. However, its role in hepatocellular carcinoma (HCC) progression remains elusive. Here, we investigate the expression and function of MTERF3 HCC. is overexpressed HCC tumor tissues higher positively correlates with poor overall survival patients. Knockdown induces dysfunction, S-G2/M cell cycle arrest apoptosis, resulting proliferation inhibition. In contrast, overexpression promotes proliferation. Mechanistically, dysfunction induced by knockdown ROS accumulation, activating p38 MAPK signaling pathway to suppress conclusion, accumulation inhibits via suggesting a promising target

Язык: Английский

Процитировано

4