Autophagy is a key lysosome-dependent degradation pathway essential for maintaining cellular homeostasis, particularly in the highly secretory pancreas. This review summarizes recent advances in autophagy, selective autophagy, and vesicle trafficking in pancreatic physiology and disease. We focus on the dual role of autophagy, which can support cellular protection and organelle quality control, but also contribute to pathology when dysregulated. We highlight emerging molecular mechanisms linking autophagy with vesicle trafficking systems, including membrane remodeling, organelle contact sites, and key regulators such as VMP1 and Beclin-1. In addition, we discuss the role of autophagy in pancreatic inflammation and cancer, emphasizing its context-dependent function. Finally, we outline recent translational approaches targeting autophagy-related pathways, including pharmacological and genetic strategies, with potential diagnostic and therapeutic relevance in pancreatic diseases.
Jakub Motor, Michał Hajt, Dastin Misiaszek et al.· International Journal of Inn...· 0 citations
Background.Major depressive disorder (MDD) is increasingly recognized as a disorder of impaired neuroplasticity. Brain-derived neurotrophic factor (BDNF) plays a central role in neuronal survival, synaptic plasticity, and antidepressant mechanisms [1–4]. Physical exercise has emerged as an effective non-pharmacological intervention capable of enhancing BDNF signaling and promoting neuroplastic adaptations [20–27].
Aim.To summarize current evidence on the role of exercise-induced BDNF signaling in mediating neuroplastic adaptations and antidepressant effects in depression.
Material and methods.A narrative review of peer-reviewed studies, including mechanistic research, randomized controlled trials, cohort studies, and meta-analyses, was conducted. Evidence from neuroscience, exercise physiology, and clinical psychiatry was integrated.
Results.Exercise increases BDNF expression through multiple biological pathways, including lactate signaling, muscle–brain crosstalk, and kynurenine metabolism [8–10]. These adaptations promote neurogenesis, synaptic plasticity, and improvements in brain connectivity [11,12,16,17]. Meta-analyses demonstrate that exercise increases circulating BDNF levels and reduces depressive symptoms [14,15,22]. Epidemiological and clinical studies indicate that higher physical activity is associated with a lower risk of depression and improved mental health outcomes [20–30].
Conclusions.BDNF appears to be a key mediator of the antidepressant effects of exercise. Current evidence supports the inclusion of structured physical activity as an evidence-based component of depression treatment, although further research is needed to optimize exercise protocols and clarify individual differences in BDNF responsiveness.
P. Turzyńska, M. Liedtke, Alicja Biskup et al.· Quality in Sport· 0 citations
