Acute respiratory infections contribute to morbidity and mortality worldwide. The common cause of this deadly disease is a virus, and one of the most commonly found is the influenza virus. Influenza viruses have several capabilities in infection, including utilizing the host\'s machinery to survive within cells and replicate safely. This review aims to examine the literature on how influenza viruses use host machinery, including endocytosis and autophagy, for their internalization and replication within cells. This review method involves a literature search by examining articles published in the PubMed and Scopus databases. The keywords used were \"Endocytosis\" OR \"Autophagy\" AND \"Influenza Virus\". Eighteen articles were included due to inclusion and exclusion criteria. GTPases switch, and V-ATPase plays a key role in the endocytic machinery hijacked by influenza viruses to enter host cells. On the other hand, LC3 and Atg5 facilitate influenza-induced apoptosis via the autophagic pathway. In conclusion, influenza viruses primarily use clathrin-mediated endocytosis to enter cells and avoid degradation during endosomal maturation by exiting endosomes for transfer to the nucleus for replication. It also uses autophagy to induce apoptosis to continue replication. The capability of the influenza viruses to hijack endocytosis and autophagy mechanisms could be critical points for further research. Therefore, we discuss how the influenza virus utilizes both endocytosis and autophagy and the approach for a new strategic therapy targeting those mechanisms.

FLOT1, a scaffold protein of lipid rafts, is involved in several biological processes, including lipid raft protein‑-dependent or clathrin‑independent endocytosis, and the formation of hippocampal synapses, amongst others. Increasing evidence has shown that FLOT1 can function as both a cancer promoter and cancer suppressor dependent on the type of cancer. FLOT1 can affect the occurrence and development of several types of cancer by affecting epithelial‑mesenchymal transition, proliferation of cancer cells, and relevant signaling pathways, and is regulated by long intergenic non‑coding RNAs or microRNAs. In the nervous system, overexpression or abnormally low expression of FLOT1 may lead to the occurrence of neurological diseases, such as Alzheimer\'s disease, Parkinson\'s disease, major depressive disorder and other diseases. Additionally, it is also associated with dilated cardiomyopathy, pathogenic microbial infection, diabetes‑related diseases, and gynecological diseases, amongst other diseases. In the present review, the structure and localization of FLOT1, as well as the physiological processes it is involved in are reviewed, and then the upstream and downstream regulation of FLOT1 in human disease, particularly in different types of cancer and neurological diseases are discussed, with a focus on potentially targeting FLOT1 for the clinical treatment of several diseases.

Since the spread of the deadly virus SARS-CoV-2 in late 2019, researchers have restlessly sought to unravel how the virus enters the host cells. Some proteins on each side of the interaction between the virus and the host cells are involved as the major contributors to this process: (1) the nano-machine spike protein on behalf of the virus, (2) angiotensin converting enzyme II, the mono-carboxypeptidase and the key component of renin angiotensin system on behalf of the host cell, (3) some host proteases and proteins exploited by SARS-CoV-2. In this review, the complex process of SARS-CoV-2 entrance into the host cells with the contribution of the involved host proteins as well as the sequential conformational changes in the spike protein tending to increase the probability of complexification of the latter with angiotensin converting enzyme II, the receptor of the virus on the host cells, are discussed. Moreover, the release of the catalytic ectodomain of angiotensin converting enzyme II as its soluble form in the extracellular space and its positive or negative impact on the infectivity of the virus are considered.

Viruses rely on host-cell machinery in order to invade host cells and carry out a successful infection. G-protein coupled receptor (GPCR)-mediated signaling pathways are master regulators of cellular physiological processing and are an attractive target for viruses to rewire cells during infection. In particular, the GPCR-associated scaffolding proteins β-arrestins and GPCR signaling effectors G-protein receptor kinases (GRKs) have been identified as key cellular factors that mediate viral entry and orchestrate signaling pathways that reprogram cells for viral replication. Interestingly, a broad range of viruses have been identified to activate and/or require GPCR-mediated pathways for infection, including polyomaviruses, flaviviruses, influenza virus, and SARS-CoV-2, demonstrating that these viruses may have conserved mechanisms of host-cell invasion. Thus, GPCR-mediated pathways highlight an attractive target for the development of broad antiviral therapies.

Here, we link approved and emerging nucleic acid-based therapies with the expanding universe of small non-coding RNAs (sncRNAs) and the innate immune responses that sense oligonucleotides taken up into endosomes. The Toll-like receptors (TLRs) 3, 7, 8, and 9 are located in endosomes and can detect nucleic acids taken up through endocytic routes. These receptors are key triggers in the defense against viruses and/or bacterial infections, yet they also constitute an Achilles heel towards the discrimination between self- and pathogenic nucleic acids. The compartmentalization of nucleic acids and the activity of nucleases are key components in avoiding autoimmune reactions against nucleic acids, but we still lack knowledge on the plethora of nucleic acids that might be released into the extracellular space upon infections, inflammation, and other stress responses involving increased cell death. We review recent findings that a set of single-stranded oligonucleotides (length of 25-40 nucleotides (nt)) can temporarily block ligands destined for endosomes expressing TLRs in human monocyte-derived dendritic cells. We discuss knowledge gaps and highlight the existence of a pool of RNA with an approximate length of 30-40 nt that may still have unappreciated regulatory functions in physiology and in the defense against viruses as gatekeepers of endosomal uptake through certain routes.

The endocytosis mechanism is a complicated system that is essential for cell signaling and survival. Megalin, a membrane-associated endocytic receptor, and its related proteins such as cubilin, the neonatal Fc receptor for IgG, and NaPi-IIa are important in receptors-mediated endocytosis. Physiologically, megalin uptakes plasma vitamins and proteins from primary urine, preventing their loss. It also facilitates tubular retrieval of solutes and endogenous components that may be involved in modulation and recovery from kidney injuries. Moreover, megalin is responsible for endocytosis of xenobiotics and drugs in renal tubules, increasing their half-life and/or their toxicity. Fluctuations in megalin expression and/or functionality due to changes in its regulatory mechanisms are associated with some sort of kidney injury. Also, it\'s an important component of several pathological conditions, including diabetic nephropathy and Dent disease. Thus, exploring the fundamental role of megalin in the kidney might help in the protection and/or treatment of multiple kidney-related diseases. Hence, this review aimed to explore the physiological roles of megalin in the kidney and their implications for kidney-related injuries.

Lipid rafts, also known as microdomains, are important components of cell membranes and are enriched in cholesterol, glycophospholipids and receptors. They are involved in various essential cellular processes, including endocytosis, exocytosis and cellular signaling. Receptors are concentrated at lipid rafts, through which cellular signaling can be transmitted. Pathogens exploit these signaling mechanisms to enter cells, proliferate and egress. However, lipid rafts also play an important role in initiating antimicrobial responses by sensing pathogens via clustered pathogen-sensing receptors and triggering downstream signaling events such as programmed cell death or cytokine production for pathogen clearance. In this review, we discuss how both host and pathogens use lipid rafts and associated proteins in an arms race to survive. Special attention is given to the involvement of the major vault protein, the main constituent of a ribonucleoprotein complex, which is enriched in lipid rafts upon infection with vaccinia virus.

As part of the leap development of high-tech, REEs have become emerging pollutants that have attracted more and more attention in our production and life. This article summarizes and discusses the distribution and detection rate of REEs in the world\'s soil and water, and briefly introduces the top five countries with rare earth reserves in the world. The focus is on the impact of REEs on plant, including the distribution of REEs in plant tissue and their bioavailability; the effect of REEs on seed germination and growth; the role of REEs in plant resistance, including abiotic stresses such as low temperature, salt stress, drought, and heavy metal stress; the response of REEs in plant physiology and biochemistry, including mineral absorption, photosynthesis, as well as the description of the substitution mechanism of REEs competing for Ca in plant cells. Summarized the possible mechanism of REEs to activate endocytosis in plants, and provided some reference and insights for revealing the mechanism of REEs affecting endocytosis from the perspective of cell and molecular biology. Finally, it points out the future development direction of rare earth and the problems considered in its application. The purpose is to provide reliable reference materials for the effective use of rare earth resources and the protection of the ecological environment.

An important motivation for the use of nanomaterials and nanoarchitectures in cancer therapy emanates from the widespread emergence of drug resistance. Although doxorubicin (DOX) induces cell cycle arrest and DNA damage by suppressing topoisomerase activity, resistance to DOX has severely restricted its anti-cancer potential. Hyaluronic acid (HA) has been extensively utilized for synthesizing nanoparticles as it interacts with CD44 expressed on the surface of cancer cells. Cancer cells can take up HA-modified nanoparticles through receptor-mediated endocytosis. Various types of nanostructures such as carbon nanomaterials, lipid nanoparticles and polymeric nanocarriers have been modified with HA to enhance the delivery of DOX to cancer cells. Hyaluronic acid-based advanced materials provide a platform for the co-delivery of genes and drugs along with DOX to enhance the efficacy of anti-cancer therapy and overcome chemoresistance. In the present review, the potential methods and application of HA-modified nanostructures for DOX delivery in anti-cancer therapy are discussed.

The definition of scavenger endothelial cells (SEC) is exclusively based on functional and structural characteristics. The following characteristics are common hallmarks for the vertebrate SEC: (a) All vertebrates examined are furnished with a population of special SEC that plays a role in the catabolism of physiologic and non-physiologic soluble waste macromolecules. (b) From the ligands that are endocytosed, SEC in all seven vertebrate classes appear to express the collagen α-chain receptor and the scavenger receptors. In addition, the hyaluronan and the mannose receptors are present on SEC of mammalia (several species) and osteichthyes (e.g., salmon and cod). It is likely that all four receptor types are present in all vertebrate classes. (c) Like liver endothelial cells (LEC) in mammals, SEC in all vertebrate classes are geared to endocytosis of soluble macromolecules, but phagocytic uptake of particles is taken care of mainly by macrophages. (d) The most primitive vertebrates (hagfish, lamprey and ray) carry their SEC in gill vessels, whereas phylogenetically younger fishes (salmon, carp, cod and plaice) carry their SEC in either kidney or heart and in all terrestrial vertebrates-SEC are found exclusively in the liver. (e) SEC of all vertebrates are localized in blood sinusoids or trabeculae that carry large amounts of slowly flowing and O2 poor blood. (f) SEC differs functionally and structurally from what is normally associated with \"conventional vascular endothelium.\"