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Topic Review
Oncogenic KRAS Mutations in Apoptosis and Autophagy Regulation
KRAS, one of the RAS protein family members, plays an important role in autophagy and apoptosis, through the regulation of several downstream effectors. In cancer cells, KRAS mutations confer the constitutive activation of this oncogene, stimulating cell proliferation, inducing autophagy, suppressing apoptosis, altering cell metabolism, changing cell motility and invasion and modulating the tumor microenvironment.
  • 594
  • 21 Jul 2022
Topic Review
Pivotal Role of Inflammation in Celiac Disease
Celiac disease (CD) is an immune mediate disease characterised by gluten dependent T-cell mediated activation, autoimmunity and derangement of the intestinal mucosa in a specific genetic background. Although the activation of the T-cells has been studied in dept, the central question remains still unanswered, namely, why a pro-inflammatory T cell response to gluten is generated instead of a regulatory response, which normally promotes oral tolerance to dietary protein antigens. There is an inflamed environment in CD intestine, enriched in cytokines, such as IL-15, or type I interferons, in which T cells tend to acquire a pro- inflammatory phenotype. The factors that create a pro-inflammatory environment in the CD intestine, leading to an expansion of gliadin-specific T cells in genetically susceptible individuals and further shifting them towards a pro-inflammatory phenotype, remain to be identified. Gluten exacerbates these constitutive alterations, by increasing the same markers already altered before the gluten introduction, both in vitro and in vivo. All these new observations add this disease “tout court” to the big family of increasing chronic inflammatory diseases where nutrients can have pro-inflammatory or anti-inflammatory effects, directly or indirectly mediated by the intestinal microbiota, where the intestine functions as a cross road for the control of the inflammation both local and at distance.
  • 431
  • 20 Jul 2022
Topic Review
Skin Aging and Cellular Senescence
Skin aging is a result of two cumulative and overlaying mechanisms denominated as intrinsic and extrinsic aging. The process of intrinsic or chronological aging affects all tissues and organs of the body, is due to the passage of time, and is influenced by genetic background. However, the skin is continuously exposed to environmental and lifestyle factors such as sunlight, pollution, cigarette smoke, and dietary habits. These factors, collectively denominated the skin exposome, are the major causes of the process of extrinsic skin aging. In addition, cellular senescence and the accumulation of senescent cells in the skin is considered as a hallmark of aging. Senescent cells contribute to the decline of tissue function and lead to age-related changes and pathologies.
  • 733
  • 19 Jul 2022
Topic Review
Major Components of Air Pollution Affecting Skin Appearance
The human skin is exposed daily to different environmental factors such as air pollutants and ultraviolet (UV) light. Air pollution is considered a harmful environmental risk to human skin and is known to promote aging and inflammation of this tissue, leading to the onset of skin disorders and to the appearance of wrinkles and pigmentation issues. Besides this, components of air pollution can interact synergistically with ultraviolet light and increase the impact of damage to the skin. 
  • 355
  • 19 Jul 2022
Topic Review
Modelling Ischaemic Stroke In Vitro
Most of the knowledge on the pathophysiological mechanisms of an ischaemic stroke is derived from animal-based in vitro and in vivo models. Over the past decades, different animal models of stroke have been developed, induced by emboli, intraluminal suture, photothrombosis or endothelin-1, typically in rodents. The rat is one of the most commonly used species in stroke research, among other reasons, due to the similarity of the cerebral vasculature and physiology with that of humans. Moreover, mice are often used, since they are helpful in unravelling the function of certain genes in the pathophysiology of stroke by means of the creation of transgenic mice. Animal stroke models have been an indispensable tool, as they can model different aspects of the complex pathophysiology of ischaemic stroke that cannot be modelled (yet) in simple in vitro models lacking intact blood vessels and blood flow. However, simplified, highly controlled in vitro systems are required and preferred when investigating specific basic mechanisms and cell type-specific responses under ischaemia-like conditions. Besides, in the context of testing potential neuroprotective compounds, working in vitro allows high-throughput screenings, even on a human-based background.
  • 336
  • 19 Jul 2022
Topic Review
Molecular Mechanisms of Parthanatos
Differential evolution of apoptosis, programmed necrosis, and autophagy, parthanatos is a form of cell death mediated by poly(ADP-ribose) polymerase 1 (PARP1), which is caused by DNA damage. PARP1 hyper-activation stimulates apoptosis-inducing factor (AIF) nucleus translocation, and accelerates nicotinamide adenine dinucleotide (NAD+) and adenosine triphosphate (ATP) depletion, leading to DNA fragmentation. The mechanisms of parthanatos mainly include DNA damage, PARP1 hyper-activation, PAR accumulation, NAD+ and ATP depletion, and AIF nucleus translocation. Parthanatos, a kind of new programmed death mode, has been put forward by Professors Ted and Valina Dawson to indicate a caspase-independent cell death subroutine that critically relies on the hyper-activation of poly(ADP-ribose) polymerase 1 (PARP1).
  • 778
  • 18 Jul 2022
Topic Review
The Role of GRP78 in Cancer Stemness
Cancer stemness is proposed to be the main cause of metastasis and tumor relapse after conventional therapy due to the main properties of cancer stem cells. These include unlimited self-renewal, the low percentage in a cell population, asymmetric/symmetric cell division, and the hypothetical different nature for absorbing external substances. As the mechanism of how cancer stemness is maintained remains unknown, further investigation into the basic features of cancer stemness is required. Many articles demonstrated that glucose-regulated protein 78 (GRP78) plays a key role in cancer stemness, suggesting that this molecule is feasible for targeting cancer stem cells.
  • 374
  • 15 Jul 2022
Topic Review
Cytoskeleton as a Potential Therapeutic Target against Glioblastoma
Glioblastomas are considered the most common and aggressive primary brain tumor in adults, with an average of 15 months’ survival rate. The treatment is surgery resection, followed by chemotherapy with temozolomide, and/or radiotherapy. Glioblastoma must have wild-type IDH gene and some characteristics, such as TERT promoter mutation, EGFR gene amplification, microvascular proliferation, among others. Glioblastomas have great heterogeneity at cellular and molecular levels, presenting distinct phenotypes and diversified molecular signatures in each tumor mass, making it difficult to define a specific therapeutic target. It is believed that the main responsibility for the emerge of these distinct patterns lies in subcellular populations of tumor stem cells, capable of tumor initiation and asymmetric division. 
  • 394
  • 15 Jul 2022
Topic Review
Ureteral Neuroendocrine Neoplasms
Primary ureteral neuroendocrine neoplasms (NENs) are rare. Small-cell neuroendocrine cancer (NEC) of the ureter is usually observed in elderly patients, and around 15 cases have been observed in females so far.
  • 369
  • 14 Jul 2022
Topic Review
Unravelling Plant Cell Death in Host Plants
Pathogens within the oomycete genus Phytophthora are among some of the most destructive plant pathogens globally, causing disease and significant losses in important agricultural and forestry crops, damaging the environment, as well as impeding attempts to mitigate climate change. What is of increasing interest is the involvement of Phytophthora effectors in regulating programed cell death (PCD)—in particular, the hypersensitive response. 
  • 394
  • 14 Jul 2022
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