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Open accessJournal ArticleDOI
Ana Maria Cuervo, Sheng Zhang 
18 Apr 2015-Cell Cycle
12 Citations
Novel function of HTT in selective autophagy.
Hence, a basic knowledge of autophagy is a prerequisite to understand the developments in the field of autophagy-related research.

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Apoptosis and ferroptosis are distinct forms of regulated cell death. Apoptosis is a well-studied process involving programmed cell death, while ferroptosis is a newly discovered type characterized by iron-dependent lipid peroxidation. Apoptosis is typically triggered by various stimuli and involves controlled cell dismantling, whereas ferroptosis is driven by the lethal accumulation of lipid peroxides in cell membranes, mediated by iron and involving lipid metabolism pathways. While apoptosis and ferroptosis were initially thought to be mutually exclusive, recent research indicates potential crosstalk between the two pathways in certain cellular contexts, suggesting a balanced interaction between them. Understanding the differences in the mechanisms and triggers of apoptosis and ferroptosis is crucial for developing targeted therapeutic strategies for various diseases.
How does igf2bp2 affect macrophages?
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IGF2BP2 plays a crucial role in modulating macrophage activation and polarization. Studies have shown that IGF2BP2 can switch macrophages from a proinflammatory (M1) phenotype to a prohealing (M2) phenotype. Additionally, IGF2BP2 mRNA expression can be induced by short-term treatment with LPS, leading to enhanced protein levels after longer exposure, indicating a regulatory role in macrophage response to stimuli. Furthermore, in the context of atherosclerosis, IGF2BP2 has been linked to foam cell formation, where its silencing reduced lipid accumulation and inflammation in macrophages. Overall, IGF2BP2 emerges as a key regulator in macrophage function, influencing their activation state and response to various environmental cues.
What is known about H19 in macrophages?
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H19, a long noncoding RNA (lncRNA), plays a significant role in macrophages in various contexts. In autoimmune liver injury, H19 is primarily expressed in type I macrophages (M1) and transported to hepatocytes via exosomes, inducing hepatocyte apoptosis. Additionally, H19 has been found to regulate the expression of the serotonin transporter (SERT) in the intestine, impacting gut health. In systemic lupus erythematosus (SLE), H19 in serum exosomes promotes macrophage proliferation and migration, affecting the release of proinflammatory factors. Moreover, in bladder cancer, exosomal H19 from M2-like tumor-associated macrophages (TAMs) regulates autophagy in cancer cells, suggesting a potential therapeutic target. Lastly, in arterial medial calcification, H19 promotes vascular smooth muscle cell calcification by interacting with miR-140-5p and modulating osteogenic differentiation.
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Liposomal doxorubicin, while offering advantages like reduced cardiotoxicity and improved tumor targeting, has some drawbacks. One limitation is the potential for fast clearance, necessitating further investigation into optimizing factors like ligand density, stability, and release rate. Additionally, specific modifications, such as sialic acid (SA) on liposomes, can impact drug retention properties and, consequently, the antitumor effect. Moreover, the intracellular uptake of doxorubicin from liposomal formulations is lower compared to free doxorubicin, potentially affecting its overall efficacy in certain cancer cell lines. These factors highlight the need for ongoing research to enhance the efficiency and effectiveness of liposomal doxorubicin delivery systems.
What are some common types of neurodegenerative diseases besides Alzheimer’s?
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Common types of neurodegenerative diseases besides Alzheimer’s include Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD), frontotemporal dementia (FTD), and multiple sclerosis. These diseases are characterized by protein misfolding, aggregation, and various pathological processes leading to neuronal dysfunction and structural deficits. Research focuses on identifying high-risk genes, disease prognostic factors, and potential therapeutic targets like autophagy stimulators, mTOR inhibitors, and neuroinflammatory signaling pathways. Machine learning algorithms are utilized for accurate classification and treatment of neurodegenerative disorders, addressing challenges like increased dimensionality and nonlinearity. The prevalence of neurodegenerative diseases is expected to rise significantly due to aging populations, emphasizing the need for better treatments with fewer side effects.
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The endoplasmic reticulum (ER) stress response plays a crucial role during embryogenesis by influencing oocyte maturation, preimplantation embryo development, and post-implantation processes. ER stress can impact protein folding, leading to the activation of unfolded protein response (UPR) pathways, which are essential for maintaining cellular homeostasis and promoting cell survival. Excessive or persistent ER stress can trigger cellular apoptosis, affecting various reproductive processes in female mammals, such as embryo implantation, preimplantation embryonic development, and placental development. Coping mechanisms like the UPR pathway are mobilized in response to ER stress, highlighting their pivotal role in the development of preimplantation embryos and the regulation of normal embryonic development. Additionally, ER stress-induced responses are critical for preventing cell death and promoting embryonic development in vitro.
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The duration of immobilization significantly impacts the rate and extent of disuse muscle atrophy (DMA). Studies show that there is variability in the rate of DMA between muscles and over the duration of immobilization, with evidence of an acute phase of atrophy and differential rates between muscle groups. Additionally, research on fibro-adipogenic progenitors (FAPs) indicates that disuse can lead to altered gene expression profiles in these cells, potentially driving senescence and contributing to muscle atrophy. Furthermore, investigations into motor unit adaptation during disuse-induced neuromuscular deficits reveal that prolonged immobilization results in a disproportionate loss of muscle strength compared to muscle size, highlighting impaired neural input and suppressed motor unit firing rates as key factors in functional decline.
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Tramadol use has been associated with the development of neurodegenerative diseases due to its neurotoxic effects. Chronic exposure to tramadol has been shown to induce neurodegeneration through various pathways such as apoptosis, autophagy, oxidative stress, and mitochondrial dysfunction. Tramadol administration can lead to cerebellum atrophy, microgliosis, neuroinflammation, and apoptotic biomarkers, along with impairments in motor coordination and neuromuscular activity. Additionally, tramadol has been linked to decreased levels of important signaling molecules in the brain, alterations in antioxidant enzyme activities, and increased oxidative stress markers, which collectively contribute to neurodegenerative processes. These findings highlight the potential risks associated with long-term tramadol use and its impact on neurological health.
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To inhibit Notch signaling in Mycobacterium tuberculosis, one effective approach is through the use of a γ-secretase inhibitor, such as DAPT. Research has shown that DAPT inhibits the Notch signaling pathway, which plays a crucial role in the regulation of immune responses during tuberculosis infection. By targeting the Notch pathway, DAPT can reduce the number of regulatory T lymphocytes (Treg), suppress pro-inflammatory responses induced by M. tuberculosis, and enhance autophagy while reducing apoptosis in infected macrophages. This inhibition of Notch signaling can lead to a decrease in immunosuppressive activities of Treg cells and promote a more effective immune response against tuberculosis, making it a potential therapeutic strategy for combating the infection.
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Vitamin D deficiency significantly impacts overall health and longevity by being associated with various age-related diseases. Deficiencies in vitamin D have been linked to cardiovascular disease, cancer, neurodegeneration, autoimmune diseases, and increased mortality rates. Moreover, low levels of vitamin D can lead to skeletal issues like osteoporosis, fractures, and muscle weakness, contributing to frailty and a higher risk of falls among the elderly. Vitamin D plays a crucial role in immune system regulation, systemic inflammatory conditions, and cardio-metabolism, emphasizing its significance in maintaining overall health and well-being. Therefore, addressing and preventing vitamin D deficiency through supplementation and adequate exposure is essential for promoting healthy aging and longevity.
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Amitriptyline, a tricyclic antidepressant, exerts its effects through various mechanisms. It has been found to enhance Ca2+-dependent desensitization and act as a trapping open-channel blocker of NMDA receptors, contributing to its efficacy against neuropathic pain. Additionally, amitriptyline inhibits endothelial cell proliferation and angiogenesis by blocking the ASM-autophagic flux axis, potentially linking it to cardiovascular side effects. In the context of fibromyalgia treatment, amitriptyline's actions on monoamine reuptake inhibition, receptor modulation, and ion channel modulation collectively alleviate pain and fatigue symptoms. Furthermore, amitriptyline interferes with autophagic flux by regulating autophagosome maturation, potentially impacting protein clearance and neurodegenerative disease risk. Lastly, connexin blockade has been shown to enhance amitriptyline's therapeutic effect in neuropathic pain, suggesting a role for connexins in modulating its action.