In contrast to stress-induced macroautophagy/autophagy that happens during nutrient deprivation and other environmental challenges, basal autophagy is thought to be an important mechanism that cells utilize for homeostatic purposes. For instance, basal autophagy is used to recycle damaged and malfunctioning organelles and proteins to provide the building blocks for the generation of new ones throughout life. In addition, specialized autophagic processes, such as lipophagy, the autophagy-induced breakdown of lipid droplets (LDs), and glycophagy (breakdown of glycogen), are employed to maintain proper energy levels in the cell. The importance of autophagy in the regulation of stem cell behavior has been the focus of recent studies. However, the upstream signals that control autophagic activity in stem cells and the precise role of autophagy in stem cells are only starting to be elucidated. In a recent publication, we described how the Egfr (epidermal growth factor receptor) pathway stimulates basal autophagy to support the maintenance of somatic cyst stem cells (CySCs) and to control lipid levels in the testis.
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http://dx.doi.org/10.1080/15548627.2020.1739450 | DOI Listing |
Int J Mol Sci
December 2024
Department of OB/GYN and REI (UniKiD), Medical Faculty and University Hospital Duesseldorf, Heinrich Heine University Duesseldorf, 40255 Duesseldorf, Germany.
To date, very little is known about how apoptosis and autophagy affect human endometrial stromal cells (ESCs), particularly how these processes might determine the depth of implantation in humans. Before investigating how apoptosis and autophagy might modulate the implantation process in an infertile population, it is necessary to clarify how these processes are regulated in healthy individuals. This study examined the protein expression related to apoptosis and autophagy in primary ESCs from fertile women, particularly in the context of decidualization and embryo contact, using Western blot analysis.
View Article and Find Full Text PDFBiosci Biotechnol Biochem
January 2025
Department of Bioresource Science, Faculty of Agriculture.
Plasmodium falciparum is a major cause of severe malaria. This protozoan infects human red blood cells and secretes large quantities of histidine-rich protein 2 (PfHRP2) into the bloodstream, making it a well-known diagnostic marker. Here, however, we identified PfHRP2 as a pathogenic factor produced by P.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Dipartimento di Scienze e Tecnologie Biologiche e Ambientali (Di.S.Te.B.A.), Università del Salento, Via Provinciale per Monteroni, 73100 Lecce, Italy.
This study examined the response to cisplatin in BxPC-3, Mia-Paca-2, PANC-1, and YAPC pancreatic cancer lines with different genotypic and phenotypic characteristics, and the mechanisms associated with their resistance. BxPC-3 and MIA-PaCa-2 cell lines were the most sensitive to cisplatin, while YAPC and PANC-1 were more resistant. Consistently, in cisplatin-treated BxPC-3 cells, the cleavage patterns of pro-caspase-9, -7, -3, and PARP-1 demonstrated that they were more sensitive than YAPC cells.
View Article and Find Full Text PDFLife Sci Alliance
March 2025
https://ror.org/003412r28 CRCT, Université de Toulouse, Inserm, CNRS, Université Toulouse III-Paul Sabatier, Centre de Recherches en Cancérologie de Toulouse, Toulouse, France
Mechanical stresses, including compression, arise during cancer progression. In solid cancer, especially breast and pancreatic cancers, the rapid tumor growth and the environment remodeling explain their high intensity of compressive forces. However, the sensitivity of compressed cells to targeted therapies remains poorly known.
View Article and Find Full Text PDFAntioxid Redox Signal
December 2024
Department of Clinical Nutrition, Guangzhou Institute of Disease-Oriented Nutritional Research, Guangzhou Red Cross Hospital of Jinan University, Guangzhou, China.
Under normal physiological conditions, Nrf2 undergoes ubiquitination and subsequent proteasome degradation to maintain its basal activity. Oxidative stress can trigger Nrf2 activation, prompting its translocation to the nucleus where it functions as a transcription factor, activating various antioxidant pathways, and conferring antioxidant properties. While extensive research has shown Nrf2's protective role in various diseases, emerging evidence suggests that Nrf2 activation can also produce harmful effects.
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