Chitosan, a cationic polysaccharide derived from the deacetylation of chitin, is widely distributed in nature. Its antibacterial activity, biocompatibility, biodegradability, and non-toxicity have given it extensive uses in medicine, food, and cosmetics. However, the significant impact of variations in the physicochemical properties of chitosan extracted from different sources on its application efficacy, as well as the considerable differences in its antimicrobial mechanisms under varying conditions, limit the full realization of its biological functions. Therefore, this paper provides a comprehensive review of the structural characteristics of chitosan, its preparation methods from different sources, its antimicrobial mechanisms, and the factors influencing its antimicrobial efficacy. Furthermore, we highlight the latest applications of chitosan and its derivatives across various fields. We found that the use of microbial extraction shows promise as a new method for producing high-quality chitosan. By analyzing the different physicochemical properties of chitosan from various sources and the application of chitosan-based materials (such as nanoparticles, films, sponges, and hydrogels) prepared using different methods in biomedicine, food, agriculture, and cosmetics, we expect these findings to provide theoretical support for the broader utilization of chitosan.

Lung carcinoma incidence and fatality rates remain among the highest on a global scale. The efficacy of targeted therapies and immunotherapies is commonly compromised by the emergence of drug resistance and other factors, resulting in a lack of durable therapeutic benefits. Ferroptosis, a distinct pattern of cell death marked by the buildup of iron-dependent lipid peroxides, has been shown to be a novel and potentially more effective treatment for lung carcinoma. However, the mechanism and regulatory network of ferroptosis are exceptionally complex, and many unanswered questions remain. In addition, research on ferroptosis in the diagnosis and treatment of lung cancer has been growing exponentially. Therefore, it is necessary to provide a thorough summary of the latest advancements in the field of ferroptosis. Here, we comprehensively analyze the mechanisms underlying the preconditions of ferroptosis, the defense system, and the associated molecular networks. The potential strategies of ferroptosis in the treatment of lung carcinoma are also highlighted. Targeting ferroptosis improves tumor cell drug resistance and enhances the effectiveness of targeted drugs and immunotherapies. These findings may shed fresh light on the diagnosis and management of lung carcinoma, as well as the development of drugs related to ferroptosis.

Diabetes mellitus (DM) is a chronic metabolic disease caused by a complex interaction of genetic and environmental factors and is characterized by persistent hyperglycemia. Long-term hyperglycemia can cause macrovascular and microvascular damage, and compromise the heart, brain, kidney, peripheral nerves, eyes and other organs, leading to serious complications. Genistein, a phytoestrogen derived from soybean, is known for its various biological activities and therapeutic properties. Recent studies found that genistein not only has hypoglycemic activity but can also decrease insulin resistance. In addition, genistein has particular activity in the prevention and treatment of diabetic complications, such as nephropathy, cardiovascular disease, osteoarthrosis, encephalopathy and retinopathy. Therefore, the purpose of this review is to summarize the latest medical research and progress of genistein in DM and related complications and highlights its potential molecular mechanisms and therapeutic targets. Meanwhile, evidence is provided for the development and application of genistein as a potential drug or functional food in the prevention and treatment of diabetes and its related complications.

The interaction between m⁶A-methylated RNA and chromatin modification remains largely unknown. We found that targeted inhibition of bromodomain-containing protein 4 (BRD4) by siRNA or its inhibitor (JQ1) significantly decreases mRNA m⁶A levels and suppresses the malignancy of breast cancer (BC) cells via increased expression of demethylase AlkB homolog 5 (ALKBH5). Mechanistically, inhibition of BRD4 increases the mRNA stability of ALKBH5 via enhanced binding between its 3′ untranslated regions (3′UTRs) with RNA-binding protein RALY. Further, BRD4 serves as a scaffold for ubiquitin enzymes tripartite motif containing-21 (TRIM21) and ALKBH5, resulting in the ubiquitination and degradation of ALKBH5 protein. JQ1-increased ALKBH5 then demethylates mRNA of extra spindle pole bodies like 1 (ESPL1) and reduces binding between ESPL1 mRNA and m⁶A reader insulin like growth factor 2 mRNA binding protein 3 (IGF2BP3), leading to decay of ESPL1 mRNA. Animal and clinical studies confirm a critical role of BRD4/ALKBH5/ESPL1 pathway in BC progression. Further, our study sheds light on the crosstalks between histone modification and RNA methylation.