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"Ding, Sheng"
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The interaction between ferroptosis and inflammatory signaling pathways
Ferroptosis is an iron-dependent regulated cell death driven by excessive lipid peroxidation. Inflammation is one common and effective physiological event that protects against various stimuli to maintain tissue homeostasis. However, the dysregulation of inflammatory responses can cause imbalance of the immune system, cell dysfunction and death. Recent studies have pointed out that activation of inflammation, including the activation of multiple inflammation-related signaling pathways, can lead to ferroptosis. Among the related signal transduction pathways, we focused on five classical inflammatory pathways, namely, the JAK-STAT, NF-κB, inflammasome, cGAS-STING and MAPK signaling pathways, and expounded on their roles in ferroptosis. To date, many agents have shown therapeutic effects on ferroptosis-related diseases by modulating the aforementioned pathways in vivo and in vitro. Moreover, the regulatory effects of these pathways on iron metabolism and lipid peroxidation have been described in detail, contributing to further understanding of the pathophysiological process of ferroptosis. Taken together, targeting these pathways related to inflammation will provide appropriate ways to intervene ferroptosis and diseases.
Journal Article
Posttranslational Modifications in Ferroptosis
Ferroptosis was first coined in 2012 to describe the form of regulated cell death (RCD) characterized by iron-dependent lipid peroxidation. To date, ferroptosis has been implicated in many diseases, such as carcinogenesis, degenerative diseases (e.g., Huntington’s, Alzheimer’s, and Parkinson’s diseases), ischemia-reperfusion injury, and cardiovascular diseases. Previous studies have identified numerous targets involved in ferroptosis; for example, acyl-CoA synthetase long-chain family member 4 (ACSL4) and p53 induce while glutathione peroxidase 4 (GPX4) and apoptosis-inducing factor mitochondria-associated 2 (AIFM2, also known as FSP1) inhibit ferroptosis. At least three major pathways (the glutathione-GPX4, FSP1-coenzyme Q10 (CoQ10), and GTP cyclohydrolase-1- (GCH1-) tetrahydrobiopterin (BH4) pathways) have been identified to participate in ferroptosis regulation. Recent advances have also highlighted the crucial roles of posttranslational modifications (PTMs) of proteins in ferroptosis. Here, we summarize the recently discovered knowledge regarding the mechanisms underlying ferroptosis, particularly the roles of PTMs in ferroptosis regulation.
Journal Article
Mitophagy-related regulated cell death: molecular mechanisms and disease implications
During oxidative phosphorylation, mitochondria continuously produce reactive oxygen species (ROS), and untimely ROS clearance can subject mitochondria to oxidative stress, ultimately resulting in mitochondrial damage. Mitophagy is essential for maintaining cellular mitochondrial quality control and homeostasis, with activation involving both ubiquitin-dependent and ubiquitin-independent pathways. Over the past decade, numerous studies have indicated that different forms of regulated cell death (RCD) are connected with mitophagy. These diverse forms of RCD have been shown to be regulated by mitophagy and are implicated in the pathogenesis of a variety of diseases, such as tumors, degenerative diseases, and ischemia‒reperfusion injury (IRI). Importantly, targeting mitophagy to regulate RCD has shown excellent therapeutic potential in preclinical trials, and is expected to be an effective strategy for the treatment of related diseases. Here, we present a summary of the role of mitophagy in different forms of RCD, with a focus on potential molecular mechanisms by which mitophagy regulates RCD. We also discuss the implications of mitophagy-related RCD in the context of various diseases.
Journal Article
Deep learning enhanced Rydberg multifrequency microwave recognition
Recognition of multifrequency microwave (MW) electric fields is challenging because of the complex interference of multifrequency fields in practical applications. Rydberg atom-based measurements for multifrequency MW electric fields is promising in MW radar and MW communications. However, Rydberg atoms are sensitive not only to the MW signal but also to noise from atomic collisions and the environment, meaning that solution of the governing Lindblad master equation of light-atom interactions is complicated by the inclusion of noise and high-order terms. Here, we solve these problems by combining Rydberg atoms with deep learning model, demonstrating that this model uses the sensitivity of the Rydberg atoms while also reducing the impact of noise without solving the master equation. As a proof-of-principle demonstration, the deep learning enhanced Rydberg receiver allows direct decoding of the frequency-division multiplexed signal. This type of sensing technology is expected to benefit Rydberg-based MW fields sensing and communication.
Rydberg atoms are sensitive to microwave signals and hence can be used to detect them. Here the authors demonstrate a Rydberg receiver enhanced by deep learning, Rydberg atoms acting as antennae, to receive, extract, and decode the multi-frequency microwave signal effectively.
Journal Article
Protein methylation functions as the posttranslational modification switch to regulate autophagy
Studies over the past decades have elucidated the critical role of autophagy in human health and diseases. Although the processes of autophagy in the cytoplasm have been well studied, the posttranscriptional and epigenetic regulation mechanisms of autophagy are still poorly understood. Protein methylation, including histone methylation and non-histone protein methylation, is the most important type of posttranscriptional and epigenetic modification. Recent studies have shown that protein methylation is associated with effects on autophagosome formation, autophagy-related protein expression, and signaling pathway activation, but the details are still unclear. Thus, it is important to summarize the current status and discuss the future directions of research on protein methylation in the context of autophagy.
Journal Article
The epigenetic regulatory mechanisms of ferroptosis and its implications for biological processes and diseases
Ferroptosis is a form of regulated cell death triggered by the iron‐dependent peroxidation of phospholipids. Interactions of iron and lipid metabolism factors jointly promote ferroptosis. Ferroptosis has been demonstrated to be involved in the development of various diseases, such as tumors and degenerative diseases (e.g., aortic dissection), and targeting ferroptosis is expected to be an effective strategy for the treatment of these diseases. Recent studies have shown that the regulation of ferroptosis is affected by multiple mechanisms, including genetics, epigenetics, posttranscriptional modifications, and protein posttranslational modifications. Epigenetic changes have garnered considerable attention due to their importance in regulating biological processes and potential druggability. There have been many studies on the epigenetic regulation of ferroptosis, including histone modifications (e.g., histone acetylation and methylation), DNA methylation, and noncoding RNAs (e.g., miRNAs, circRNAs, and lncRNAs). In this review, we summarize recent advances in research on the epigenetic mechanisms involved in ferroptosis, with a description of RNA N6‐methyladenosine (m6A) methylation included, and the importance of epigenetic regulation in biological processes and ferroptosis‐related diseases, which provides reference for the clinical application of epigenetic regulators in the treatment of related diseases by targeting ferroptosis. Ferroptosis is a form of iron‐dependent regulated cell death driven by lipid peroxidation. Current studies have revealed that iron metabolism, lipid metabolism, and redox system jointly regulate ferroptosis. In this review, we highlight epigenetic mechanisms including histone modifications, DNA methylation, noncoding RNAs, and RNA m6A modifications in ferroptosis regulation, which provides potential therapeutic targets for ferroptosis‐related diseases.
Journal Article
Phase Diagram and Self-Organizing Dynamics in a Thermal Ensemble of Strongly Interacting Rydberg Atoms
Far-from-equilibrium dynamics that lead to self-organization are highly relevant to complex dynamical systems not only in physics but also in life, earth, and social sciences. However, it is challenging to find systems with sufficiently controllable parameters that allow quantitatively modeling of emergent properties. Here, we study a nonequilibrium phase transition and observe signatures of self-organized criticality in a dilute thermal vapor of atoms optically excited to strongly interacting Rydberg states. Electromagnetically induced transparency provides excellent control over the population dynamics and enables high-resolution probing of the driven-dissipative dynamics, which also exhibits phase bistability. Increased sensitivity compared to previous work allows us to reconstruct the complete phase diagram, including in the vicinity of the critical point. We observe that interaction-induced energy shifts and enhanced decay only occur in one of the phases above a critical Rydberg population. This case limits the application of generic mean-field models; however, a modified, threshold-dependent approach is in qualitative agreement with experimental data. Near threshold, we observe self-organized dynamics in the form of population jumps that return the density to a critical value.
Journal Article
Endometriosis alters brain electrophysiology, gene expression and increases pain sensitization, anxiety, and depression in female mice
Endometriosis is an estrogen-dependent inflammatory disorder among reproductive-aged women associated with pelvic pain, anxiety, and depression. Pain is characterized by central sensitization; however, it is not clear if endometriosis leads to increased pain perception or if women with the disease are more sensitive to pain, increasing the detection of endometriosis. Endometriosis was induced in mice and changes in behavior including pain perception, brain electrophysiology, and gene expression were characterized. Behavioral tests revealed that mice with endometriosis were more depressed, anxious and sensitive to pain compared to sham controls. Microarray analyses confirmed by qPCR identified differential gene expression in several regions of brain in mice with endometriosis. In these mice, genes such as Gpr88, Glra3 in insula, Chrnb4, Npas4 in the hippocampus, and Lcn2 in the amygdala were upregulated while Lct, Serpina3n (insula), and Nptx2 (amygdala) were downregulated. These genes are involved in anxiety, locomotion, and pain. Patch clamp recordings in the amygdala were altered in endometriosis mice demonstrating an effect of endometriosis on brain electrophysiology. Endometriosis induced pain sensitization, anxiety, and depression by modulating brain gene expression and electrophysiology; the effect of endometriosis on the brain may underlie pain sensitization and mood disorders reported in women with the disease. Summary Sentence Endometriosis disrupts brain gene expression and electrophysiology, inducing anxiety, depression, and pain sensitization in mice.
Journal Article