List of Articles Autophagy

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  1 - The interaction between Helicobacter pylori and autophagy: A putative mechanism involved in gastric carcinogenesis
  Marzieh Esmaeilzadeh Abbas Yadegar Farshid Kafilzadeh Mohammad Kargar Hamid Asadzadeh Aghdaei
  Helicobacter pylori is a Gram-negative bacterium that colonizes the gastric tissue of more than half of the world's population and is the major risk factor for the development of gastric cancer.  H. pylori is the most common bacterial pathogen in humans, and there More

  Helicobacter pylori is a Gram-negative bacterium that colonizes the gastric tissue of more than half of the world's population and is the major risk factor for the development of gastric cancer.  H. pylori is the most common bacterial pathogen in humans, and there is a significant association  between H. pylori infection and gastric cancer. Autophagy is a protective process used by  eukaryotic cells to maintain cell homeostasis and defend against the attack of pathogenic    microbes. H. pylori can induce autophagy in epithelial cells of the stomach and professional  phagocytes such as macrophages and dendritic cells. Tumor inhibitory proteins including   phosphatases, PTEN, P53, and retinoblastoma protein have a positive effect on autophagy   regulation. In comparison, oncogenic products such as BCL-2 and AKT/TOR pathways play an inhibitory role on autophagy. However, the relationship between regulation of autophagy and   tumorigenesis is still unclear. During H. pylori infection and after the induction of autophagy, the bacterium can escape this process by downregulation of autophagy-related proteins, and/or use the autophagosome as a suitable niche for intracellular survival. In addition, autophagy can cause cell survival or cell death through the gastric cancer process. In conclusion, the role of H. pylori  infection in induction or inhibition of autophagy process, and its impact on gastric carcinogenic related pathways are a matter of controversy, which need further studies to understand the   interactions between the microbe and autophagy.  Manuscript profile
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  2 - The effect of high-intensity interval training on the content of autophagy proteins (BECLIN1 and AMBRA1) in the skeletal muscle of aged rats
  Hamid Khodaverdi Neda Aghaei Bahmanbeglou saeedeh Shadmehri
  Introduction: One of the complications associated with aging is the reduction of muscle volume, which is caused by defects in cellular pathways such as autophagy. Exercises can be a key factor in reversing or increasing this complication; Therefore, the aim of this rese More

  Introduction: One of the complications associated with aging is the reduction of muscle volume, which is caused by defects in cellular pathways such as autophagy. Exercises can be a key factor in reversing or increasing this complication; Therefore, the aim of this research is the effect of high-intensity interval training (HIIT) on the content of autophagy proteins (BECLIN1 and AMBRA1) in the skeletal muscle of aged rats. Materials and Methods: The current research is of experimental-fundamental type, in which 12, 20-month-old male Sprague-Dawley rats with an average weight of 400±30 grams were randomly divided into 2 groups: 1) control (6 head) and 2) HIIT (6 head). The HIIT training program consisted of 8 weeks and 3 sessions per week with an intensity of 85-90% of VO2max. After 48 hours after the last training session, the EDL muscle tissue of the rats was removed. Data analysis Data were analysed through independent t-test in SPSS version 27 and GraphPad Prism version 2.2.10 software. The significance level was less than p≥0.05. Results: Eight weeks of HIIT training increased BECLIN1 protein intracellular content (P=0.0001) and decreased AMBRA1 protein intracellular content (P=0.0001) in EDL muscle of aged rats. Conclusion: Considering the conflicting results in the content of BECLIN1 and AMBRA1 proteins, it suggests that the adaptive responses of HIIT differ in the regulation of the autophagy pathway. Manuscript profile