Quercetin, a flavonoid found in vegetables and fruits, has been extensively studied for its health benefits and disease management. Its role in the prevention of various pathogenesis has been well-documented, primarily through its ability to inhibit oxidative stress, inflammation, and enhance the endogenous antioxidant defense mechanisms. Electronic databases such as Google Scholar, Scopus, PubMed, Medline, and Web of Science were searched for information regarding quercetin and its role in various pathogeneses. The included literature comprised experimental studies, randomized controlled trials, and epidemiological studies related to quercetin, while editorials, case analyses, theses, and letters were excluded. It has been reported to have a wide range of health benefits including hepatoprotective, antidiabetic, anti-obesity, neuroprotective, cardioprotective, wound healing, antimicrobial, and immunomodulatory effects, achieved through the modulation of various biological activities. Additionally, numerous in vitro and in vivo studies have shown that quercetin’s efficacies in cancer management involve inhibiting cell signaling pathways, such as inflammation, cell cycle, and angiogenesis, activating cell signaling pathways including tumor suppressor genes, and inducing apoptosis. This review aims to provide a comprehensive understanding of the health benefits of quercetin in various pathogeneses. Additionally, this review outlines the sources of quercetin, nanoformulations, and its applications in health management, along with key findings from important clinical trial studies. Limited clinical data regarding quercetin’s safety and mechanism of action are available. It is important to conduct more clinical trials to gain a deeper understanding of the disease-preventive potential, mechanisms of action, safety, and optimal therapeutic dosages. Furthermore, more research based on nanoformulations should be performed to minimize/overcome the hindrance associated with bioavailability, rapid degradation, and toxicity.

Lycopene, a carotenoid commonly found in tomatoes, is an emerging compound with a noteworthy role in the prevention and treatment of various pathologies. Evidence from in vitro and in vivo models indicates that lycopene plays an imperative role in disease management through the regulation of oxidative stress, inflammation, and the modulation of various biological processes. Its role containing nephroprotective, hepatoprotective, cardioprotective, and neuroprotective properties, anti-arthritis, anti-obesity, and wound healing has been documented. Its significant role in cancer management through modulation of inflammation, angiogenesis, apoptosis, cell cycle, and PI3/Akt pathways has been properly described. This review aims to provide a comprehensive overview of the role of lycopene in the management of pathogenesis. The review further evaluates the current evidence regarding the synergistic interactions of lycopene with other bioactive compounds and drugs and highlights the potential of emerging nanoformulation strategies to improve its bioavailability and therapeutic efficacy in disease management. However, this compound shows some limitations, particularly its low bioavailability and poor water solubility, which hinder its therapeutic benefit in disease management. For a better understanding of its mechanisms of action, safety considerations, potential drug interactions, and optimal dosages, further detailed studies based on both preclinical and clinical data are needed. This further investigation is essential to reveal the maximum potential benefit of lycopene in disease management.

Invariant natural killer T (iNKT) cells are a unique lymphocyte subset that bridge innate and adaptive immunity through recognition of glycolipid antigens presented by CD1d. Upon activation by ligands such as α-galactosylceramide (α-GalCer), iNKT cells rapidly secrete cytokines, including IFN-γ and TNF-α, thereby activating dendritic cells, natural killer (NK) cells, and cytotoxic T lymphocytes (CTLs) to promote antitumor immunity. Despite their therapeutic promise, clinical translation has been limited by rapid α-GalCer clearance, induction of iNKT cell anergy following repeated stimulation, and the immunosuppressive tumor microenvironment (TME). Recent advances in lipid-engineered nanoparticle systems offer solutions to these challenges by improving ligand stability, enhancing antigen-presenting cell targeting, and enabling controlled release that sustains Th1-biased activation while reducing anergy. Liposomal and polymer-based nano-formulations enhance bioavailability and promote more durable IFN-γ-mediated responses. In parallel, chimeric antigen receptor (CAR)-engineered iNKT cells provide antigen-specific tumor targeting while preserving intrinsic CD1d-restricted immunomodulatory functions, demonstrating encouraging safety and efficacy in early-phase studies. Combination strategies further strengthen iNKT-based immunotherapy. Integration with chemotherapy, immune checkpoint inhibitors such as anti-PD-1 and anti-CTLA-4, and cytokine support enhances effector activation, counteracts TME-induced suppression, and improves therapeutic outcomes. However, challenges remain, including optimization of dosing, control of off-target immune activation, scalable manufacturing, and long-term safety evaluation. Collectively, the convergence of nanotechnology, CAR engineering, and rational combination approaches establishes iNKT cell-based therapy as a promising next-generation immunotherapeutic strategy. Continued refinement of delivery systems, genetic engineering platforms, and translational protocols may enable durable immune reprogramming and improved clinical outcomes in resistant and immunosuppressive cancers.

Background and Objectives: Osteoporosis (OP) is a prevalent condition among postmenopausal women, with an estimated 40% of Saudi women affected. Concurrently, type 2 diabetes mellitus (T2DM) is highly prevalent in the Qassim region, affecting 45% of individuals aged 40 and older. Despite conflicting evidence regarding the impact of T2DM on bone health, its role in OP development remains uncertain. Materials and Methods: This study investigates site-specific bone mineral density (BMD) variations and their metabolic correlations in postmenopausal Saudi women with T2DM. A cross-sectional study included 250 postmenopausal Saudi women, 100 without diabetes (Group 1) and 150 with diabetes (Group 2), matched for age, menopausal duration, and body mass index (BMI). BMD at the femoral neck (FN) and lumbar spine (LS) was assessed using dual-energy X-ray absorptiometry (DXA). Biochemical markers, including parathyroid hormone (PTH), alkaline phosphatase (ALP), estrogen, calcium, and HbA1c, were assessed. Statistical analyses, including chi-square tests, t-tests, ANOVA, Pearson correlation, and multivariate regression, evaluated BMD variations and biochemical associations. Results: Patients with diabetes exhibited significantly higher FN T-scores than those without diabetes (p = 0.001), while LS T-scores showed no significant difference. BMD distribution (normal, osteopenia, OP) did not differ between the groups (p > 0.05). FN T-scores correlated positively with parathyroid hormone (PTH) and alkaline phosphatase (ALP) levels, reduced estrogen, and prolonged menopause duration (p < 0.01) but were inversely associated with estrogen levels and menopause duration (p < 0.01). Conclusions: No significant association was found between HbA1c and BMD. Additionally, BMI demonstrated a protective effect on FN BMD. T2DM appears to influence bone metabolism without directly causing OP in postmenopausal women. Aging, menopause duration, metabolic markers (PTH, ALP, estrogen), and BMI play crucial roles in BMD variations, with a protective effect of BMI. These findings underscore the importance of site-specific BMD assessment and metabolic profiling in postmenopausal women with diabetes. Further longitudinal research is needed to elucidate the underlying mechanisms affecting bone health in postmenopausal women with diabetes.

The following references [181] have been retracted and should be removed from the original publication