Topic Review
Sarcopenia Pathophysiology
The pathophysiology of sarcopenia has multifactorial causes. Some cellular and molecular mechanisms have been suggested to be involved that include protein homeostasis imbalance, inflammation, mitochondrial dysfunction, and satellite cell dysfunction. These factors do not independently cause sarcopenia but interact with each other to cause sarcopenia.
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Topic Review
Role of Sensory Innervation in Corneal Epithelial Renewal
Corneal clarity is required for vision, and blindness occurs when the cornea becomes opaque. The cornea is covered by unique transparent epithelial cells that serve as an outermost cellular barrier bordering between the cornea and the external environment. Corneal sensory nerves protect the cornea from injury by triggering tearing and blink reflexes, and are also thought to regulate corneal epithelial renewal via unknown mechanism(s). When protective corneal sensory innervation is absent due to infection, trauma, intracranial tumors, surgery, or congenital causes, permanent blindness results from repetitive epithelial microtraumas and failure to heal. The condition is termed neurotrophic keratopathy (NK), with an incidence of 5:10,000 people worldwide.
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Topic Review
TDP-43 Role in Chromatin Remodeling and Transcription
TDP-43 gained momentum in the neurodegeneration field when it was first discovered that almost all amyotrophic lateral sclerosis (ALS) cases and as many as half of frontotemporal dementia (FTD) cases present pathological ubiquitinated inclusions of TDP-43. Its involvement in chromatin silencing and nuclear/cytoplasmic shuttling constitute convergent key findings from several biological screens, and several crucial epigenetic factors appear to be able to modify TDP-43-induced degeneration. TDP-43 activity at the chromatin level and its implication in the regulation of DNA transcription and stability -such as DNA repair and regulation of retrotransposons activity- are further supported by a continuously growing amount of studies.
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Topic Review
Netosis in Brief
Netosis is a complex and fascinating cellular process that plays a pivotal role in our immune defense system. It involves the formation and release of neutrophil extracellular traps (NETs) composed of chromatin and antimicrobial proteins. These NETs act as sophisticated snares, capturing and neutralizing various pathogens, including bacteria, fungi, and parasites. The process begins with chromatin decondensation, mediated by enzymes like PAD4, allowing the extrusion of chromatin from the nucleus into the cytoplasm. Subsequent rupture of the nuclear envelope leads to NET formation and their release into the extracellular environment. While netosis is essential for immune defense, dysregulation can contribute to autoimmune diseases, inflammatory disorders, and even thrombosis. Understanding netosis opens doors to potential therapeutic interventions targeting this intricate cellular mechanism.
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Topic Review
Ferroptosis in Brief
Ferroptosis is a newly discovered, iron-dependent form of programmed cell death characterized by the lethal accumulation of lipid peroxides within cell membranes. This process, distinct from apoptosis or necrosis, is driven by disruptions in cellular iron homeostasis and subsequent oxidative damage. Ferroptosis plays a pivotal role in various physiological processes and diseases, including cancer, neurodegenerative disorders, and ischemic injuries. Understanding the mechanisms and regulation of ferroptosis holds promise for the development of novel therapeutic strategies, making it a burgeoning field of research in cell biology and medicine with potential applications across a wide range of health-related challenges.
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Topic Review
Necroptosis in Brief
Necroptosis is a recently discovered form of programmed cell death that has gained significant attention in scientific and medical research. This review provides a comprehensive exploration of necroptosis, covering its molecular mechanisms and regulatory pathways. Key components like receptor-interacting protein kinases (RIPK1 and RIPK3) and mixed lineage kinase domain-like (MLKL) are discussed in detail, along with their roles in necroptotic cell death. The research also highlights the physiological functions of necroptosis in development, tissue maintenance, and immune response, as well as its involvement in diseases such as neurodegenerative disorders, inflammatory conditions, and cancer. Additionally, it touches on potential therapeutic interventions and the future outlook of necroptosis research.
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Topic Review
Pyroptosis in Brief
This comprehensive entry delves into the intricate world of pyroptosis, a captivating phenomenon in cellular biology and immunology. It provides a comprehensive exploration of pyroptosis, from its historical context to its multifaceted mechanisms, regulatory intricacies, physiological functions, and its relevance in health and disease. Pyroptosis represents a unique blend of programmed cell death and inflammatory responses, challenging conventional categorizations and sparking curiosity across diverse scientific disciplines. The research highlights the central role of inflammasomes in orchestrating pyroptosis and its interplay with innate immunity. Overall, this entry offers a brief dive into the fascinating world of pyroptosis, its implications, and its potential for future research and therapeutic applications.
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Topic Review
Chaperone-Mediated Autophagy in Peritumoral Pericyte during Glioblastoma Multiforme
Glioblastoma multiforme (GB) is an aggressive cancer with poor prognosis as it is one of the most difficult cancers to treat. Glioblastoma (GB) cells physically interact with peritumoral pericytes (PCs) present in the brain microvasculature. These interactions facilitate tumor cells to aberrantly increase and benefit from chaperone-mediated autophagy (CMA) in the PC. GB-induced CMA leads to major changes in PC immunomodulatory phenotypes, which, in turn, support cancer progression. 
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Topic Review
MOB in Cytokinesis, Cell Architecture and Tissue Homeostasis
The Monopolar spindle One Binder protein (MOB) family proteins are constituted by highly conserved eukaryote kinase signal adaptors that are often essential both for cell and organism survival. Historically, MOB family proteins have been described as kinase activators participating in Hippo and Mitotic Exit Network/Septation Initiation Network (MEN/SIN) signaling pathways that have central roles in regulating cytokinesis, cell polarity, cell proliferation and cell fate to control organ growth and regeneration. In metazoans, MOB proteins act as central signal adaptors of the core kinase module MST1/2, LATS1/2, and NDR1/2 kinases that phosphorylate the YAP/TAZ transcriptional co-activators, effectors of the Hippo signaling pathway. MOBs have been shown to also have non-kinase partners and to be involved in cilia biology, indicating that its activity and regulation is more diverse than expected.
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Topic Review
Non-Coding RNAs
The mammalian transcriptome is highly complex and includes a large number of small non-coding RNAs (sncRNAs) and long noncoding RNAs (lncRNAs). Here, the biogenesis pathways of the three classes of sncRNAs, namely short interfering RNAs (siRNAs), microRNAs (miRNAs) and PIWI-interacting RNAs (piRNAs) are discussed. These ncRNAs have been extensively studied and are involved in pathways leading to specific gene silencing and the protection of genomes against virus and transposons, for example. Also, lncRNAs have emerged as pivotal molecules for the transcriptional and post-transcriptional regulation of gene expression which is supported by their tissue-specific expression patterns, subcellular distribution, and developmental regulation.
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