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Aging is the result of the accumulation of a wide variety of molecular and cellular damage over time. This has been associated with a number of features termed hallmarks of aging, including genomic instability, loss of proteostasis, telomere attrition, dysregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and impaired intercellular communication. On the other hand, sirtuins are enzymes with an important role in aging and life extension, of which humans have seven paralogs (SIRT1 to SIRT7). SIRT7 is the least studied sirtuin to date, but it has been reported to serve important functions, such as promoting ribosomal RNA expression, aiding in DNA damage repair, and regulating chromatin compaction. Several studies have established a close relationship between SIRT7 and age-related processes, but knowledge in this area is still scarce. Therefore, the purpose of this review was to analyze how SIRT7 is associated with each of the hallmarks of aging, as well as with some of age-associated diseases, such as cardiovascular diseases, obesity, osteoporosis, and cancer.

Sirtuin 6 (SIRT6), a member of the class III histone deacetylase (HDAC) family, is crucial for the maintenance of general health and is associated with increased life expectancy and resistance to age-related diseases such as cancer and metabolic disorders. A comparative analysis of the SIRT6 gene in Ashkenazi Jewish (AJ) centenarians and noncentenarian controls found a distinct allele, centSIRT6, enriched in the centenarian group. This allele features 2 linked substitutions, N308K and A313S, and exhibits enhanced functions, including more efficient suppression of LINE1 retrotransposons, improved repair of DNA double-strand breaks, and increased efficiency in cancer cell killing. Notably, centSIRT6 shows lower deacetylase activity but higher mono-adenosine diphosphate (ADP) ribosyl transferase activity compared with the wild-type enzyme. This study used several bioinformatics tools to explore the structural changes caused by the N308K and A313S substitutions in centSIRT6 and to elucidate how these alterations contribute to changes in the enzymatic activities of SIRT6. The results indicate that these mutations reduce the structural flexibility of centSIRT6, thus weakening its interactions with acetyl-lysine but strengthening its interactions with ADP-ribose. This research provides useful information for future experimental studies to further investigate the molecular mechanisms of centSIRT6.

There is a growing awareness that the large number of environmental pollutants we are exposed to on a daily basis are causing major health problems. Compared to traditional studies that focus on individual pollutants, there are relatively few studies on how pollutants mixtures interact. Several studies have reported a relationship between environmental pollutants and the development of cancer, even when pollutant levels are below toxicity reference values. The possibility of synergistic interactions between different pollutants could explain how even low concentrations can cause major health problems. These intricate that molecular interactions can occur through a wide variety of mechanisms, and our understanding of the physiological effects of mixtures is still limited. The purpose of this paper is to discuss recent reports that address possible synergistic interactions between different types of environmental pollutants that could promote cancer development. Our literature studies suggest that key biological pathways are frequently implicated in such processes. These include increased production of reactive oxygen species, activation by cytochrome P450, and aryl hydrocarbon receptor signaling, among others. We discuss the need to understand individual pathological vulnerability not only in relation to basic genetics and gene expression, but also in terms of measurable exposure to contaminants. We also mention the need for significant improvements in future studies using a multitude of disciplines, such as the development of high‐throughput study models, better tools for quantifying pollutants in cancer patients, innovative pharmacological and toxicological studies, and high‐efficiency computer analysis, which allow us to analyze the molecular mechanisms of mixtures. Plain Language Summary In general, every day we are exposed to many pollutants at the same time, and each pollutant can interact with others in different ways. Notably, two or more pollutants can interact and enhance their effects through a phenomenon called synergy and this would explain why, even at low concentrations, pollutants can have important health effects. Several studies have reported a link between environmental pollutants and cancer. Thus, our review of the literature suggests that synergy phenomena between pollutants can alter key points in cells and facilitate cancer development. Similarly, we mention the complications and needs to assess these complex interactions in subsequent studies. Key Points There are an increasing number of reports on the synergetic actions of pollutants in cancer Mixtures of pollutants can interact (synergy/antagonism) affecting different biological pathways Key pathways frequently implicated in synergetic action are reactive oxygen species, cytochrome P450, and aryl hydrocarbon receptor

Coronavirus disease 2019 (COVID-19) is a disease caused by infection with the SARS-CoV-2 virus and has represented one of the greatest challenges humanity has faced in recent years. The virus can infect a large number of organs, including the lungs and upper respiratory tract, brain, liver, kidneys, and intestines, among many others. Although the greatest damage occurs in the lungs, the kidneys are not exempt, and acute kidney injury (AKI) can occur in patients with COVID-19. Indeed, AKI is one of the most frequent and serious organic complications of COVID-19. The incidence of COVID-19 AKI varies widely, and the exact mechanisms of how the virus damages the kidney are still unknown. For this reason, the purpose of this review was to assess current findings on the pathogenesis, clinical features, therapy, and mortality of COVID-19 AKI.

Background: Atypical carcinoid of the thymus is an exceptionally rare neuroendocrine tumor originating from neuroendocrine cells within the thymus. These tumors often present with no symptoms or with nonspecific clinical signs, making early diagnosis particularly challenging. Despite their rarity, atypical carcinoids are clinically significant due to their aggressive nature and relatively poor prognosis. Early detection and appropriate management are therefore crucial to improving patient outcomes. Results: In this report, we present the case of a 64-year-old patient in whom an atypical carcinoid of the thymus was incidentally discovered following a thoracic computed tomography scan performed for unrelated reasons. Imaging revealed a suspicious anterior mediastinal mass, which was subsequently surgically resected. Histopathological examination, supported by immunohistochemical analysis, confirmed the diagnosis of an atypical carcinoid of the thymus. The tumor demonstrated coexpression of epithelial and neuroendocrine markers, consistent with this rare entity. Conclusions: This case adds to the limited body of literature on atypical carcinoid of the thymus and highlights the importance of considering this diagnosis when evaluating anterior mediastinal masses. It also underscores the value of thorough radiological and pathological assessment in identifying early-stage disease, which may significantly influence prognosis and therapeutic strategies.

Small nucleolar RNAs (snoRNAs) are short non-coding RNAs that are abundant in the nucleoli of eukaryotic cells and play a crucial role in various aspects of ribosomal RNA (rRNA) maturation, including modifications such as 2′-O-methylation or pseudouridylation. On the other hand, Giardia duodenalis is a microaerophilic, flagellated, binucleate protozoan responsible for causing giardiasis. Although numerous snoRNAs have been detected in Giardia, their investigation remains limited. Nevertheless, they have been found to play a crucial role in the rRNA precursor processing pathway and influence other cellular functions. In addition, it has been proposed that some microRNAs are generated from these snoRNAs through excision by the Giardia endoribonuclease Dicer. These microRNAs are believed to contribute to the regulation of antigenic variation, which allows the parasite to evade the host immune response. Specifically, they play a role in modulating variant-specific surface proteins (VSPs) and other cysteine-rich surface antigens (CSAs). The main objective of this study was to bring together the available data on snoRNAs in Giardia, uncovering their functions in various processes and their importance on a global scale. In addition, the research delved into potential microRNAs speculated to originate from snoRNAs, exploring their impact on cellular processes.

Circular RNAs (circRNA) are covalently closed single-stranded RNA molecules that act as important regulators of gene expression through different mechanisms. Meanwhile, cancer stem cells (CSCs) are a small subpopulation of cells, with properties similar to normal stem cells that arise during the development of cancer and support tumor growth, induce resistance to therapy, and are responsible for metastatic spread. Since the elimination of CSCs is an important goal of cancer treatment, the circRNAs that participate in regulating gene expression and signaling pathways linked to CSCs have aroused attention in recent years, especially because it has been suggested that these molecules may function as therapeutic targets and/or clinical biomarkers. Thus, the proposal of this work is to enumerate a series of circRNAs that have been shown to play a relevant role in CSCs and explain in detail the molecular regulatory mechanisms that they establish to perform that function.

Humanity has always sought to live longer and for this, multiple strategies have been tried with varying results. In this sense, G protein-coupled receptors (GPCRs) may be a good option to try to prolong our life while maintaining good health since they have a substantial participation in a wide variety of processes of human pathophysiology and are one of the main therapeutic targets. In this way, we present the analysis of a series of GPCRs whose activity has been shown to affect the lifespan of animal and human models, and in which we put a special interest in describing the molecular mechanisms involved. Our compilation of data revealed that the mechanisms most involved in the role of GPCRs in lifespan are those that mimic dietary restriction, those related to insulin signaling and the AMPK and TOR pathways, and those that alter oxidative homeostasis and severe and/or chronic inflammation. We also discuss the possibility of using agonist or antagonist drugs, depending on the beneficial or harmful effects of each GPCR, in order to prolong people's lifespan and healthspan.

FMS-like tyrosine kinase 3 (FLT3) is a proto-oncogene involved in crucial steps of haematopoiesis such as proliferation, differentiation and survival. In recent years, FLT3 has been an important marker in different haematological malignancies, highlighting in acute myeloid leukaemia, where FLT3 mutations have been associated with the clinical prognosis, treatment and survival of patients. The most common form of FLT3 mutation is an internal tandem duplication (ITD) that promotes ligand-independent auto-phosphorylation and constitutive activation of the receptor. FLT3–ITD has been strongly associated with a bad prognosis, leukocytosis, high blast counts, increased risk of relapse and shorter overall survival. In order to improve the clinical condition of FLT3–ITD-positive patients, several FLT3 inhibitors have been developed showing variable results. Currently, the main challenges to be overcome are the different forms of resistance to FLT3 inhibitors. Thus, the purpose of this review is to present, in a general way, the current role that FLT3–ITD mutation plays in patients with AML, with a particular emphasis on the molecular mechanisms associated with clinical prognosis, treatment, and survival of patients.

Contrasting with several theories of ageing, bats are mammals with remarkable longevity despite their high metabolic rate, living on average three times more than other mammals of equal size. The question of how bats live a long time has attracted considerable attention, and they have thus been related to immortal fantasy characters like Dracula in the novel by Bram Stoker. Several ecological and physiological features, such as reduction in mortality risks, delayed sexual maturation and hibernation, have been linked to bats’ long lifespan. However, there is still very little information about the molecular mechanisms associated with the longevity of bats. In this regard, the present work tries to summarize current knowledge about how bats can live for so long, taking into consideration nutritional factors, oxidative metabolism, protein homeostasis, stress resistance, DNA repair, mitochondrial physiology and cancer resistance.