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PE is a life-threatening pregnancy disorder that can lead to adverse events for both the fetus and the mother. Autophagy is a cellular process involved in cellular renovation and maintaining homeostasis. There is a growing body of evidence suggesting that autophagy in trophoblasts plays a significant role in the development and pathogenesis of PE. However, the exact mechanisms are not yet fully understood. This article provides an overview of recent evidence regarding the role of autophagy in trophoblast invasion, vascular remodelling, inflammation, immune response, and maternal factors in the context of PE. It is believed that impaired or excessive autophagy can contribute to placental ischaemia and hypoxia, thereby exacerbating PE progression. Therefore, understanding the molecular mechanisms that regulate autophagy in PE is crucial for the development of targeted therapeutic interventions in the future.
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http://dx.doi.org/10.1111/cpr.70102 | DOI Listing |
Crit Rev Food Sci Nutr
September 2025
Hunan Key Laboratory of Deep Processing and Quality Control of Cereals and Oils, State Key Laboratory of Utilization of Woody Oil Resource, College of Food Science and Engineering, Central South University of Forestry and Technology, Changsha, Hunan, China.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a condition that results from metabolic disorders. In addition to genetic factors, irregular and high-energy diets may also significantly contribute to its pathogenesis. Dietary habits can profoundly alter the composition of gut microbiota and metabolites.
View Article and Find Full Text PDFCell Mol Biol (Noisy-le-grand)
September 2025
Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Despite significant advancements in the treatment of non-small cell lung cancer (NSCLC) using conventional therapeutic methods, drug resistance remains a major factor contributing to disease recurrence. In this study, we aimed to explore the potential benefits of combining PI3K inhibition with Cisplatin in the context of NSCLC-derived A549 cells. Human non-small cell lung cancer A549 cells were cultured and treated with BKM120, cisplatin, or their combination.
View Article and Find Full Text PDFMol Biol Rep
September 2025
Dr. B. R. Ambedkar Centre for Biomedical Research North Campus , University of Delhi, 110007, Delhi, India.
Background: Standard treatment for glioblastoma includes chemotherapy, alkylating agents such as temozolomide (TMZ); however, MGMT resistance leads to recurrence. Demethoxycurcumin (DMC) has been reported to inhibit cancer cell growth, induce apoptosis, and prevent metastasis in different cancer models. We investigated the DMC-induced apoptosis and autophagy via inhibition of the AKT/mTOR pathway in human glioma U87MG and T98G cell lines.
View Article and Find Full Text PDFJ Asthma
September 2025
Department of Acupuncture and Moxibustion, the First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou 310006, China.
Objective: In traditional Chinese medicine, asthma is associated with deficiencies in Lung Qi, Spleen Qi, and Kidney Qi. This study investigated the therapeutic mechanism of point application therapy focusing on the acupoints Feishu (BL13), Pishu (BL20), and Shenshu (BL23) for asthma treatment.
Methods: An asthma model was established in Wistar rats via intraperitoneal ovalbumin injection combined with nebulisation.
Adv Sci (Weinh)
September 2025
State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University, Yangling, Shaanxi, 712100, P. R. China.
Mounting evidence indicates that viruses exploit elevated reactive oxygen species (ROS) levels to promote replication and pathogenesis, yet the mechanistic underpinnings of this viral strategy remain elusive for many viral systems. This study uncovers a sophisticated viral counter-defense mechanism in the Cryphonectria hypovirus 1 (CHV1)-Fusarium graminearum system, where the viral p29 protein subverts host redox homeostasis to overcome antiviral responses. That p29 directly interacts with and inhibits the enzymatic activity of fungal NAD(P)H-dependent FMN reductase 1 (FMR1), leading to increased ROS accumulation and subsequent autophagy activation is demonstrated.
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