Cordycepin Activates Autophagy to Suppress FGF9-induced TM3 Mouse Leydig Progenitor Cell Proliferation DOI Open Access
Su-Zhen Wu, Yu-Yan Lan,

Chia‐Fu Chen

и другие.

Cancer Genomics & Proteomics, Год журнала: 2024, Номер 21(6), С. 630 - 644

Опубликована: Окт. 28, 2024

Background/Aim: Fibroblast growth factor 9 (FGF9) is a member of the human FGF family known for its pivotal roles in various biological processes, such as cell proliferation, tissue repair, and male sex determination including testis formation. Cordycepin, bioactive compound found Cordyceps sinensis, exhibits potent antitumor effects by triggering apoptosis and/or autophagy pathways. Our research has unveiled that FGF9 promotes proliferation tumorigenesis MA-10 mouse Leydig tumor cells, phenomena are effectively countered cordycepin through induction. Moreover, we have observed FGF9-mediated stimulation TM3 progenitor prompting an investigation into potential inhibitory effect on under treatment. Hence, hypothesized induces death via FGF9-treated cells. Materials Methods: cells were treated with FGF9, flow cytometry, immunofluorescent plus western blotting assays used to determine how regulated Results: findings reveal restricts viability colony formation while inducing morphological alterations associated Surprisingly, fails elicit expression key apoptotic markers, suggesting alternate mechanism action. Although certain autophagy-related proteins remains unaltered, significant up-regulation LC3-II, indicative autophagy, cordycepin-treated influence. inhibition chloroquine reverses cordycepin-induced death, highlighting crucial role this process. Conclusion: study demonstrates activates induce treatment conditions.

Язык: Английский

Roles of HSP70 in autophagic protection of cardiomyocytes induced by heat acclimation: A review DOI
Yue Huang, Guoyu Li, Shuwan Wang

и другие.

International Journal of Biological Macromolecules, Год журнала: 2025, Номер unknown, С. 142984 - 142984

Опубликована: Апрель 1, 2025

Язык: Английский

Процитировано

0

Autophagy activity in cardiac fibroblasts at the early stages of cardiac dysfunction induced by pressure overload DOI Open Access
К. В. Дергилев, Yu.D. Goltseva, З. И. Цоколаева

и другие.

Russian Cardiology Bulletin, Год журнала: 2025, Номер 20(1), С. 13 - 13

Опубликована: Апрель 14, 2025

Despite advancements in investigation of cardiac fibrosis mechanisms, molecular and cellular regulation this process remains insufficiently explored. In context, examination novel targets capable regulating the state fibroblasts their profibrotic properties becomes a pivotal area research. These processes include autophagy as an evolutionary conservative mechanism contributing to maintenance homeostasis through utilization macromolecules organelles via lysosomal degradation pathway. The objective was investigate at early stages dysfunction caused by pressure overload. Experimental studies showed that modelling transverse aortic constriction promotes overload with cardiomyocyte hypertrophy, perivascular interstitial accumulation collagen. morphological changes were accompanied reduced activity tissue. A detailed bioinformatic analysis transcriptome single cells revealed not expression genes associated total pool its subpopulations. Thus, demonstrated differences specialized response heart compared myocardial cell pool. No change is probably favor suppression adaptation tissue new conditions functioning. Autophagy diagnostic marker progression requires confirmation additional studies.

Язык: Английский

Процитировано

0

Cordycepin Activates Autophagy to Suppress FGF9-induced TM3 Mouse Leydig Progenitor Cell Proliferation DOI Open Access
Su-Zhen Wu, Yu-Yan Lan,

Chia‐Fu Chen

и другие.

Cancer Genomics & Proteomics, Год журнала: 2024, Номер 21(6), С. 630 - 644

Опубликована: Окт. 28, 2024

Background/Aim: Fibroblast growth factor 9 (FGF9) is a member of the human FGF family known for its pivotal roles in various biological processes, such as cell proliferation, tissue repair, and male sex determination including testis formation. Cordycepin, bioactive compound found Cordyceps sinensis, exhibits potent antitumor effects by triggering apoptosis and/or autophagy pathways. Our research has unveiled that FGF9 promotes proliferation tumorigenesis MA-10 mouse Leydig tumor cells, phenomena are effectively countered cordycepin through induction. Moreover, we have observed FGF9-mediated stimulation TM3 progenitor prompting an investigation into potential inhibitory effect on under treatment. Hence, hypothesized induces death via FGF9-treated cells. Materials Methods: cells were treated with FGF9, flow cytometry, immunofluorescent plus western blotting assays used to determine how regulated Results: findings reveal restricts viability colony formation while inducing morphological alterations associated Surprisingly, fails elicit expression key apoptotic markers, suggesting alternate mechanism action. Although certain autophagy-related proteins remains unaltered, significant up-regulation LC3-II, indicative autophagy, cordycepin-treated influence. inhibition chloroquine reverses cordycepin-induced death, highlighting crucial role this process. Conclusion: study demonstrates activates induce treatment conditions.

Язык: Английский

Процитировано

0