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Regulation of the capacity of the core autophagy machinery also affects selective autophagy.
This work solves the long-standing enigma of how IRGM controls autophagy.
An understanding of the role of autophagy in energy homeostasis could help us better appreciate how autophagy determines cell fate under stressful conditions or pathological processes.
We illustrate that autophagy induction and the components required vary by the nature of the induction signal and type of cell and do not always require canonical members of the autophagy signaling pathway.
The present results showed that autophagy could be induced by H2S, which was verified by autophagic ultrastructural observation and LC3-I/LC3-II conversion.

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How does exposure to PM2.5 impact the expression of miR125b-5p in human cells?
5 answers
Exposure to PM2.5 has been shown to impact the expression of miR-125b-5p in human cells. Studies have demonstrated that PM2.5 exposure significantly downregulates miR-149-5p, which is a microRNA associated with inflammatory responses in COPD and other conditions. This downregulation of miR-149-5p is linked to the activation of inflammatory pathways such as MAPK and NF-κB signaling in response to PM2.5 exposure, leading to increased expression of pro-inflammatory cytokines like IL-1β, IL-6, IL-8, and TNF-α. Therefore, exposure to PM2.5 can disrupt the expression of miR-149-5p, contributing to inflammatory responses in human cells, highlighting a potential molecular mechanism underlying the impact of PM2.5 on cellular health.
What are the potential future treatments for Alzheimer's disease based on current research?
5 answers
Based on current research, potential future treatments for Alzheimer's disease include targeting beta-amyloid and tau protein, stem cell-based therapies, non-invasive brain stimulation techniques, and dietary/lifestyle interventions. Additionally, treatments like Salubrinal, Amentoflavone, Latrepirdine, and compounds like NMN, UA, and AC show promise in alleviating ER stress, pyroptosis, inducing autophagy, and promoting mitophagy. Herbal medicines and stem cell therapies are also being explored as potential treatments for AD, with stem cell transplantation studies showing promise in both preclinical and clinical approaches. Nanoparticles are being investigated for targeted drug delivery to the central nervous system, while natural compounds like alkaloids, terpenoids, flavonoids, and curcumin are showing potential therapeutic benefits against AD. Current symptomatic therapies include cholinesterase inhibitors, glutamate receptor antagonists, and natural medicines with anti-inflammatory properties.
What are the underlying mechanisms that contribute to skin aging being considered a metabolic disorder?
5 answers
Skin aging is increasingly recognized as a metabolic disorder due to various underlying mechanisms. Metabolic reprogramming in dermal fibroblasts, characterized by enhanced fatty acid oxidation and reduced glycolysis, is linked to the aging process. Additionally, perturbations in cell metabolism, such as altered glycolysis and glycerolipid biosynthesis, are associated with impaired skin function in aging individuals. The mTORC2 pathway, known for regulating aging processes, is upregulated in intrinsic and photo-induced skin aging, leading to NF-κB activation. Mitochondrial dysfunction and oxidative stress are also implicated in skin photoaging, highlighting the role of mitochondria in the aging process and suggesting potential interventions for skin aging. These findings collectively emphasize the intricate relationship between metabolism and skin aging, positioning skin aging as a metabolic disorder influenced by various cellular and molecular pathways.
How does rifaximin influence cognitive function?
5 answers
Rifaximin, a non-absorbable antibiotic, exerts beneficial effects on cognitive function through various mechanisms. Studies show that rifaximin reduces neuroinflammation in the hippocampus, normalizes glutamate receptor expression, and improves spatial memory. Additionally, rifaximin protects against cognitive impairment induced by circadian rhythm disruption by modulating gut microbiota, enhancing intestinal barrier integrity, and suppressing inflammatory responses. Furthermore, rifaximin has been found to influence functional brain connectivity, particularly in the insular cortex, affecting cognitive flexibility and memory processing. Moreover, rifaximin's neuroprotective effects involve enhancing autophagy, inhibiting amyloid-β accumulation, and promoting neuronal protection in the hippocampus. Overall, rifaximin's multifaceted actions on neuroinflammation, gut microbiota, brain connectivity, and autophagy contribute to its positive impact on cognitive function in various conditions.
Does ROS causes benefit for skeletal muscle through mTORC1?
5 answers
Reactive oxygen species (ROS) play a dual role in skeletal muscle through mTORC1 signaling. ROS generated during physical exercise induce beneficial effects by activating mTORC1, promoting muscle adaptations like increased glucose uptake and hypertrophy. Conversely, excessive ROS levels can lead to oxidative stress, disrupting muscle integrity and function. Studies show that ATM activates TSC2 via LKB1 and AMPK in response to ROS, leading to mTORC1 suppression and induction of autophagy, a process crucial for cellular survival. Inhibition of mTORC1 by ROS-induced ATM signaling can be rescued by rapamycin, highlighting the intricate balance between ROS, mTORC1, and autophagy in skeletal muscle physiology. Therefore, ROS can indeed confer benefits to skeletal muscle through mTORC1 signaling, but the levels must be tightly regulated to prevent detrimental effects.
What is the physiological role of PAX5?
4 answers
PAX5 plays a crucial role in various physiological processes related to B-cell development and function. It acts as a positive transcription factor for GINS1 expression, controls gene expression profiles essential for cellular processes like viability and differentiation, and is pivotal for B-cell commitment and maintenance. In mature B cells, PAX5 promotes humoral immunity by facilitating differentiation and survival through posttranscriptional down-regulation of PTEN expression. Additionally, PAX5 has been found to have a negative role in osteoclastogenesis, inhibiting osteoclast differentiation and bone resorption. These diverse functions highlight the multifaceted role of PAX5 in regulating various aspects of B-cell biology, immunity, and bone metabolism.
What is PD3?
5 answers
PD3 refers to different entities based on the contexts provided. In the first context, PD3 is a fluorescent probe designed for PDEδ inhibition, aiding in the visualization and pharmacological inhibition of oncogenic proteins. In the second context, PD3 is the designation for a phase II clinical trial named ROCK, focusing on preoperative robotic radiosurgery for early breast cancer patients. Additionally, in the third context, PD3 is a novel class of dual BRD4/ULK3 inhibitors developed to target triple negative breast cancer, showing effectiveness in limiting TNBC viability by inhibiting MYC expression and autophagy. Therefore, PD3 encompasses a fluorescent probe for PDEδ inhibition, a clinical trial designation, and a class of inhibitors targeting TNBC through dual epigenetic/autophagy inhibition.
What are the molecular mechanisms that contribute to the development and progression of endometrial cancer?
5 answers
The development and progression of endometrial cancer involve various molecular mechanisms. Mutations in CTNNB1, encoding β-catenin, play a role in driving progression, particularly in a subset of patients with worsened progression-free survival. Additionally, miRNAs are implicated in regulating genes related to carcinogenesis, serving as potential diagnostic and prognostic biomarkers. The cancer microenvironment, including signals from stromal cells and extracellular matrix, influences malignancy, invasion, and metastasis in endometrial cancer, impacting treatment sensitivity and overall prognoses. SNORD15B acts as an oncogene by targeting the TRIM25/P53 complex, affecting P53 localization and promoting tumorigenicity in endometrial cancer cells. Furthermore, the PI3K/AKT/mTOR pathway and angiogenesis-related molecules are closely associated with the pathogenesis of endometrial cancer, highlighting their role in disease development.
What is the role of insulin receptor recycling in regulating glucose uptake in muscle cells?
5 answers
Insulin receptor recycling plays a crucial role in regulating glucose uptake in muscle cells. Upon insulin binding to its receptor, intracellular glucose transporters, such as GLUT4, are redistributed to the plasma membrane, allowing for increased glucose uptake. This process involves multiple signaling pathways and molecular mechanisms. The insulin receptor catalyzes the tyrosine phosphorylation of insulin receptor substrate (IRS) proteins, which activate the phosphatidylinositol 3-kinase (PI3K) pathway and protein kinases like Akt and atypical protein kinase C. Additionally, the insulin receptor phosphorylates the adapter protein APS, leading to the activation of the G protein TC10, which influences cellular processes such as actin cytoskeleton changes and assembly of the exocyst complex. These pathways converge to control the recycling of GLUT4 and its translocation to the plasma membrane, facilitating glucose uptake.
How does the interaction between PM 2.5 exposure and HMGB1 expression contribute to exacerbations in asthmat?
5 answers
The interaction between PM2.5 exposure and HMGB1 expression contributes to exacerbations in asthma. PM2.5 exposure activates the Notch signaling pathway, leading to Th1/Th2 immune imbalance and aggravation of asthma. Additionally, PM2.5 exposure disrupts airway epithelial cells and elicits airway inflammation and remodeling. Furthermore, PM2.5 exposure induces the expression of platelet-derived growth factor-AB (PDGF-AB), PDGF-BB, and transforming growth factor-β1 (TGF-β1) via high-mobility group box 1 (HMGB1) receptor for advanced glycation end products (RAGE) signaling. HMGB1-RAGE signaling pathway contributes to airway remodeling observed in patients with COPD. Therefore, the interaction between PM2.5 exposure and HMGB1 expression plays a role in exacerbations of asthma by promoting immune imbalance, airway inflammation, and remodeling.
What is pold2 in cancer?
5 answers
PLOD2, also known as procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2, plays an oncogenic role in various cancers, including colorectal carcinoma (CRC). It is upregulated in CRC and its higher expression is associated with poorer survival. PLOD2 promotes CRC proliferation, invasion, and metastasis in vitro and in vivo. It interacts with USP15, stabilizing it in the cytoplasm and activating the phosphorylation of AKT/mTOR, thereby promoting CRC progression. PLOD2 is also expressed differently in normal tissues and significantly highly expressed in most tumors compared with normal tissues. Its expression is negatively correlated with the prognosis of several tumors, including gastric cancer. PLOD2 is significantly associated with tumor infiltration, immune checkpoint expression, and immune microenvironment scores, suggesting its role in tumor immunity. In addition, PLOD2 is significantly overexpressed in gastric cancer. Overall, PLOD2 plays a significant role in tumorigenesis and may serve as a potential biomarker for diagnosis and prognosis in cancers.