Cellular senescence regulates aging, tissue maintenance, and disease progression through the Senescence-Associated Secretory Phenotype (SASP), a secretory profile of cytokines, chemokines, growth factors, and matrix-remodeling enzymes. While transient SASP aids wound healing, its chronic activation drives inflammation, fibrosis, and tumorigenesis. This review examines SASP’s molecular regulation, dual roles in health and pathology, and therapeutic potential. The following two main strategies are explored: senescence clearance, which eliminates SASP-producing cells, and SASP modulation, which refines secretion to suppress inflammation while maintaining regenerative effects. Key pathways, including NF-κB, C/EBPβ, and cGAS-STING, are discussed alongside pharmacological, immunotherapeutic, gene-editing, and epigenetic interventions. SASP heterogeneity necessitates tissue-specific biomarkers for personalized therapies. Challenges include immune interactions, long-term safety, and ethical considerations. SASP modulation emerges as a promising strategy for aging, oncology, and tissue repair, with future advancements relying on multi-omics and AI-driven insights to optimize clinical outcomes.

The rapid progress of antibiotic resistance among bacteria has prompted serious medical concerns regarding how to manage multidrug-resistant (MDR) bacterial infections. One emerging strategy to combat antibiotic resistance is the use of antimicrobial peptides (AMPs), which are amino acid chains that act as broad-spectrum antimicrobial molecules and are essential parts of the innate immune system in mammals, fungi, and plants. AMPs have unique antibacterial mechanisms that offer benefits over conventional antibiotics in combating drug-resistant bacterial infections. Currently, scientists have conducted multiple studies on AMPs for combating drug-resistant bacterial infections and found that AMPs are a promising alternative to conventional antibiotics. On the other hand, bacteria can develop several tactics to resist and bypass the effect of AMPs. Therefore, it is like a battle between the bacterial community and the AMPs, but who will win? This review provides thorough insights into the development of antibiotic resistance as well as detailed information about AMPs in terms of their history and classification. Furthermore, it addresses the unique antibacterial mechanisms of action of AMPs, how bacteria resist these mechanisms, and how to ensure AMPs win this battle. Finally, it provides updated information about FDA-approved AMPs and those that were still in clinical trials. This review provides vital information for researchers for the development and therapeutic application of novel AMPs for drug-resistant bacterial infections.

Background and Aim: The human gut microbiome plays a crucial role in maintaining health. Artificial sweeteners, also known as non-nutritive sweeteners (NNS), have garnered attention for their potential to disrupt the balance of the gut microbiome. This review explores the complex relationship between NNS and the gut microbiome, highlighting their potential benefits and risks. By synthesizing current evidence, we aim to provide a balanced perspective on the role of AS in dietary practices and health outcomes, emphasizing the need for targeted research to guide their safe and effective use. Methods: A comprehensive literature review was conducted through searches in PubMed and Google Scholar, focusing on the effects of artificial sweeteners on gut microbiota. The search utilized key terms including “Gut Microbiome”, “gut microbiota”, “Eubiosis”, “Dysbiosis”, “Artificial Sweeteners”, and “Nonnutritive Sweeteners”. Results: NNS may alter the gut microbiome, but findings remain inconsistent. Animal studies often report a decrease in beneficial bacteria like Bifidobacterium and Lactobacillus, and an increase in harmful strains such as Clostridium difficile and E. coli, potentially leading to inflammation and gut imbalance. Disruptions in short-chain fatty acid (SCFA) production and gut hormone signaling have also been observed. However, human studies generally show milder or no significant changes, highlighting the limitations in translating animal model findings directly to humans. Differences in study design, dosage, exposure time, and sweetener type likely contribute to these varied outcomes. Conclusions: While NNS offer certain benefits, including reduced caloric intake and improved blood sugar regulation, their impact on gut microbiome health raises important concerns. The observed reduction in beneficial bacteria and the rise in pathogenic strains underscore the need for caution in NNS consumption. Furthermore, the disruption of SCFA production and metabolic pathways illustrates the intricate relationship between diet and gut health.

Anlotinib, a novel receptor tyrosine kinase inhibitor that is taken orally, targets several RTKs and is authorized as a third-line treatment for patients with advanced non-small cell lung cancer (NSCLC). Anlotinib is also used in combination with immunotherapy or chemotherapy for advanced NSCLC. We aimed to explore the efficacy and safety of anlotinib-based regimens in NSCLC treatment, focusing on combination therapies. We also addressed challenges that hinder oncologists from using it, such as toxicity and resistance mechanisms. A systematic approach involves searching the National Institute of Health PubMed, Scopus, MedLine, and Web of Science databases up to April 2024. Relevant studies were identified and analyzed for their methodologies, outcomes, and patient characteristics. Findings revealed that numerous effective combination regimens, such as anlotinib with platinum-based chemotherapy and anlotinib combined with PD-1 blockades, have shown positive results in terms of progression-free survival (PFS), overall survival (OS), and objective response rate (ORR). On the other hand, NSCLC treatment faces hurdles due to drug resistance and its toxicity profile. These challenges underscore the need for continued research and optimization of treatment strategies.

Ferroptosis, characterized by iron dependency and lipid peroxidation, has emerged as a key mechanism underlying neurodegeneration in rare neurological disorders. These conditions, often marked by significant therapeutic gaps and high unmet medical needs, present unique challenges for intervention development. This review examines the involvement of ferroptosis in rare neurological disease pathogenesis, focusing on its role in oxidative damage and neuronal dysfunction. We explore recent pharmacological advancements, including iron chelators, lipid peroxidation blockers, and antioxidant-based strategies, designed to target ferroptosis. While these approaches show promise, challenges such as disease heterogeneity, limited diagnostic tools, and small patient cohorts hinder progress. Furthermore, we discuss the translational and regulatory barriers to implementing ferroptosis-based therapies in clinical practice. By addressing these obstacles and fostering innovative solutions, this review underscores the potential of ferroptosis-targeting strategies to revolutionize treatment paradigms for rare neurological disorders.