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Lung cancer therapeutic resistance, especially chemoresistance, is a key issue in the management of this malignancy. Despite the development of novel molecularly targeted drugs to promote therapeutic efficacy, 5‐year survival of lung cancer patients is still dismal. Molecular studies through the recent years have fortunately presented multiple genes and signaling pathways, which contribute to lung cancer chemoresistance, providing a better perception of the biology of tumor cells, as well as the molecular mechanisms involved in their resistance to chemotherapeutic agents. Among those mechanisms, transfer of extracellular vesicles, such as exosomes, between cancer cells and the surrounding noncancerous ones is considered as an emerging route. Exosomes can desirably function as signaling vesicles to transmit multiple molecules from normal cells to cancer cells and their microenvironment, or vice versa. Using this ability, exosomes may affect the cancer cells' chemoresistance/chemosensitivity. Recently, noncoding RNAs (esp. microRNAs and long noncoding RNAs), as key molecules transferred by exosomes, have been reported to play a substantial role in the process of drug resistance, through modulation of various proteins and their corresponding genes. Accordingly, the current review principally aims to highlight exosomal micro‐ and long noncoding RNAs involved in lung cancer chemoresistance. Moreover, major molecular mechanisms, which connect corresponding RNA molecules to drug resistance, will briefly be addressed, for better clarifying of possible roles of exosomal noncoding RNAs in promoting the effectiveness of lung cancer therapy.

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Obesity is associated with changes in the resolution of acute inflammation that contribute to the clinical complications. The exact mechanisms underlying unresolved inflammation in obesity are not fully understood. Adipocyte death leads to pro-inflammatory adipose tissue macrophages, stimulating additional adipocyte apoptosis. Thus, a complex and tightly regulated process to inhibit inflammation and maintain homeostasis after adipocyte apoptosis is needed to maintain health. In normal condition, a specialized phagocytic process (efferocytosis) performs this function, clearing necrotic and apoptotic cells (ACs) and controlling inflammation. For efficient and continued efferocytosis, phagocytes must internalize multiple ACs in physiological conditions and handle the excess metabolic burden in adipose tissue. In obesity, this control is lost and can be an important hallmark of the disease. In this regard, the deficiency of efferocytosis leads to delayed resolution of acute inflammation and can result in ongoing inflammation, immune system dysfunction, and insulin resistance in obesity. Hence, efficient clearance of ACs by M2 macrophages could limit long-term inflammation and ensue clinical complications, such as cardiovascular disease and diabetes. This review elaborates upon the molecular mechanisms to identify efferocytosis regulators in obesity, and the mechanisms that can improve efferocytosis and reduce obesity-related complications, such as the use of pharmacological agents and regular exercise.

Gliomas make up virtually 80% of all lethal primary brain tumors and are categorized based on their cell of origin. Glioblastoma is an astrocytic tumor that has an inferior prognosis despite the ongoing advances in treatment modalities. One of the main reasons for this shortcoming is the presence of the blood-brain barrier and blood-brain tumor barrier. Novel invasive and non-invasive drug delivery strategies for glioblastoma have been developed to overcome both the intact blood-brain barrier and leverage the disrupted nature of the blood-brain tumor barrier to target cancer cells after resection—the first treatment stage of glioblastoma. Exosomes are among non-invasive drug delivery methods and have emerged as a natural drug delivery vehicle with high biological barrier penetrability. There are various exosome isolation methods from different origins, and the intended use of the exosomes and starting materials defines the choice of isolation technique. In the present review, we have given an overview of the structure of the blood-brain barrier and its disruption in glioblastoma. This review provided a comprehensive insight into novel passive and active drug delivery techniques to overcome the blood-brain barrier, emphasizing exosomes as an excellent emerging drug, gene, and effective molecule delivery vehicle used in glioblastoma therapy. Supplementary Information The online version contains supplementary material available at 10.1007/s12035-023-03365-0.