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Topic Review
IL-6 Cytokines and EMP
Epithelial–mesenchymal plasticity (EMP) plays critical physiological roles during embryonic development, postnatal growth and epithelial homeostasis, but it is also involved in a number of pathological conditions, including wound repair, fibrosis, inflammation and cancer. EMP has been intimately linked with most, if not all, of the steps during cancer development and progression (e.g., migration, invasion, immune escape, drug resistance and metastatic dissemination). Cytokines from the interleukin 6 (IL-6) family play fundamental roles in mediating tumour-promoting inflammation within the tumour microenvironment. In general, IL-6 cytokines activate EMP processes, fostering the acquisition of mesenchymal features in cancer cells. Here, we will summarise all the relevant literature related to all members of the IL-6 family and EMP.
  • 471
  • 29 Mar 2022
Topic Review
IIIG9 in Cancer and Other Pathologies
The identification of new proteins that regulate the function of one of the main cellular phosphatases, protein phosphatase 1 (PP1), is essential to find possible pharmacological targets to alter phosphatase function in various cellular processes, including the initiation and development of multiple diseases. IIIG9 is a regulatory subunit of PP1 initially identified in highly polarized ciliated cells. In addition to its ciliary location in ependymal cells, researchers showed that IIIG9 has extraciliary functions that regulate the integrity of adherens junctions.
  • 491
  • 01 Dec 2022
Topic Review
Hypoxia-Related Unfolded Protein Response in Tumor Microenvironment
The tumor microenvironment (TME) is a dynamic network that is created by blood vessels, lymphatic vessels, fibroblasts, immune cells as well as components such as the extracellular matrix (ECM) that establishes a “friendly ecosystem” for cancer cells. Hypoxia induces a cellular adaptive response that elevates the expression of the transcription factors called hypoxia-inducible factors (HIFs) that activate the global gene expression changes in both non-malignant and cancer cells. While most of the studies in this area have focused on the canonical responses to hypoxia, a better understanding is needed for the complex molecular changes that are found in the hypoxic TME. These changes include the deregulation of endoplasmic reticulum (ER) homeostasis, and the subsequent perturbations in protein folding and secretion. The potential for erratic protein folding can also lead to another specialized stress response signaling pathway called the unfolded protein response (UPR). The UPR promotes survival during hypoxia by restoring the endoplasmic and mitochondrial homeostasis, but at times, it can also inhibit the cancer cell’s survival. The maturation of transmembrane and secretory proteins that include proangiogenic receptors and ligands as well as ECM remodeling enzymes takes place in the ER. 
  • 251
  • 19 Oct 2022
Topic Review
Hypoxia-Inducible Factors in Osteogenesis
As central mediators of homeostasis, hypoxia-inducible transcription factors (HIFs) can allow cells to survive in a low-oxygen environment and are essential for the regulation of osteogenesis and skeletal repair.
  • 539
  • 13 Oct 2022
Topic Review
Hypoxia-Inducible Factors and Immunosenescence
Hypoxia activates hypoxia-related signaling pathways controlled by hypoxia-inducible factors (HIFs). HIFs represent a quick and effective detection system involved in the cellular response to insufficient oxygen concentration.
  • 185
  • 23 Aug 2023
Topic Review
Hypoxia-Inducible Factor-1α
Aging is one of the hottest topics in biomedical research. Advances in research and medicine have helped to preserve human health, leading to an extension of life expectancy. However, the extension of life is an irreversible process accompanied by the development of aging-related conditions such as weakness, slower metabolism, and stiffness of vessels. It also debated that aging can be considered an actual disease with aging-derived comorbidities, including cancer or cardiovascular disease. Currently, cardiovascular disorders, including atherosclerosis, are considered premature aging and represent the first causes of death in developed countries, accounting for 31% of annual deaths globally. Emerging evidence has identified hypoxia-inducible factor-1α as a critical transcription factor with an essential role in aging-related pathology, in particular, regulating cellular senescence associated with cardiovascular aging.
  • 747
  • 04 Aug 2021
Topic Review
Hypoxia-Associated Long Non-Coding RNAs in Breast Cancer
Breast cancer is the leading cause of cancer-related deaths in women worldwide. Long non-coding RNAs are newly described molecules that have extensive roles in breast cancer. Emerging reports have shown that there is a strong link between these RNAs and the hypoxic response of breast cancer cells, which may be an important factor for enhanced tumoral progression.
  • 329
  • 26 May 2022
Topic Review
Hypoxia in the Cell Cycle
The cell cycle is an important cellular process whereby the cell attempts to replicate its genome in an error-free manner.
  • 735
  • 01 Jul 2021
Topic Review
Hypoxia in Cardiovascular Diseases
Heart valve diseases are a major contributor to cardiovascular morbidity and mortality worldwide. They affect more than 13% of the population aged over 75 years old and occur when any type of the four heart valves (tricuspid, pulmonic, mitral, and aortic valves) is damaged. Calcific aortic valve disease (CAVD) is defined as a slowly progressing condition that ranges from mild valve aortic sclerosis to severe calcifying aortic valve stenosis. This progression manifests in approximately 2% of individuals over 65 years old annually.
  • 302
  • 20 Jul 2023
Topic Review
Hyperthermia
Hyperthermia is one of the severe acute adverse effects that can be caused by the ingestion of recreational drugs, such as methcathinones. The effect of hyperthermia on neurotoxicity is currently not known. The primary aim of our study was therefore to investigate the effects of hyperthermia (40.5 °C) on the neurotoxicity of methcathinone (MC), 4-chloromethcathinone (4-CMC), and 4-methylmethcathinone (4-MMC) in SH-SY5Y cells. We found that 4-CMC and 4-MMC were cytotoxic (decrease in cellular ATP and plasma membrane damage) under both hyper- (40.5 °C) and normothermic conditions (37 °C), whereby cells were more sensitive to the toxicants at 40.5 °C. 4-CMC and 4-MMC impaired the function of the mitochondrial electron transport chain and increased mitochondrial formation of reactive oxygen species (ROS) in SH-SY5Y cells, which were accentuated under hyperthermic conditions. Hyperthermia was associated with a rapid expression of the 70 kilodalton heat shock protein (Hsp70), which partially prevented cell death after 6 h of exposure to the toxicants. After 24 h of exposure, autophagy was stimulated by the toxicants and by hyperthermia but could only partially prevent cell death. In conclusion, hyperthermic conditions increased the neurotoxic properties of methcathinones despite the stimulation of protective mechanisms. These findings may be important for the understanding of the mechanisms and clinical consequences of the neurotoxicity associated with these compounds.
  • 805
  • 29 Oct 2020
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