Abnormal energy metabolism, as one of the important hallmarks of cancer, was induced by multiple carcinogenic factors and tumor-specific microenvironments. It comprises aerobic glycolysis, de novo lipid biosynthesis, and glutamine-dependent anaplerosis. Considering that metabolic reprogramming provides various nutrients for tumor survival and development, it has been considered a potential target for cancer therapy. Cannabinoids have been shown to exhibit a variety of anticancer activities by unclear mechanisms. This paper first reviews the recent progress of related signaling pathways (reactive oxygen species (ROS), AMP-activated protein kinase (AMPK), mitogen-activated protein kinases (MAPK), phosphoinositide 3-kinase (PI3K), hypoxia-inducible factor-1alpha (HIF-1α), and p53) mediating the reprogramming of cancer metabolism (including glucose metabolism, lipid metabolism, and amino acid metabolism). Then we comprehensively explore the latest discoveries and possible mechanisms of the anticancer effects of cannabinoids through the regulation of the above-mentioned related signaling pathways, to provide new targets and insights for cancer prevention and treatment.

Acetone (C₃H₆O) gas in the exhaled breath of diabetic patients can be used as an important biomarker for the painless and noninvasive diagnosis of diabetes mellitus. In this paper, based on the density functional theory (DFT), the adsorption behaviors of pristine and single-atom transition metal (X = Sc, Ti, V, and Cr)-doped InP₃ surfaces (denoted as X-InP₃) toward C₃H₆O molecule were examined to explore the potential of these two-dimensional (2D) materials as a sensitive sensor for acetone gas. The calculation results indicate the unfavorable detection property for the pristine 2D-InP₃ surface upon acetone with an unsatisfied gas response (12.4%). The introduction of a single-atom transition metal (Sc, Ti, V, and Cr) into the InP₃ layer has significantly improved the adsorption capacity toward the C₃H₆O molecule. Owing to the high gas response values (-98.0%, 393.3%, and 393.3%), the Ti-InP₃, V-InP₃, and Cr-InP₃ layers show their superiority in C₃H₆O detection at room temperature, in which Ti-InP₃ achieves recycle use through heating at 698 K. Sc-InP₃ is unsuitable for C₃H₆O sensing with a poor response (8.1%). Our work first gives a theoretical predication about the adsorption and sensitive detection performance of pristine and single-atom transition metal (Sc, Ti, V, and Cr)-doped InP₃ upon acetone, which may provide an emerging kind of sensing material for the noninvasive diagnosis of diabetes mellitus indicated by acetone gas.

Tetracycline is a low-cost broad-spectrum antibiotic and widely used in medicine and aquaculture. Its residues are usually released into the environment through wastewater, which may lead to the spread of antibiotic resistance genes and pose ecological risks. To address this environmental issue, a hierarchical lignin-derived porous carbon (LPHC) was synthesized using renewable biomass lignin as the precursor through a combined phosphoric acid-activated hydrothermal pretreatment. The resulting LPHC was used to effectively remove tetracycline from aqueous solutions. Characterization results indicated that LPHC had a high specific surface area (1157.25 m²·g⁻¹), a well-developed micro-mesoporous structure, and abundant surface oxygen-containing functional groups, which enhanced its interaction with target pollutants. Adsorption experiments showed that LPHC exhibited excellent adsorption performance for tetracycline, with a maximum adsorption capacity of 219.81 mg·g⁻¹. The adsorption process conformed to the Langmuir isotherm model, indicating that monolayer chemical adsorption was dominant. Mechanism analysis further confirmed that the adsorption process was controlled by multiple synergistic interactions, including pore filling, π-π electron donor–acceptor interactions, hydrogen bonding, and electrostatic attraction. This work proposes a feasible strategy to convert waste biomass into high-performance and environmentally friendly adsorbents, which provides technical feasibility for sustainable water purification technologies.

Curcumin, a natural polyphenol derived from turmeric, functions as a potent exogenous antioxidant and exhibits a range of benefits in the prevention and management of metabolic diseases. Despite its extremely low systemic bioavailability, curcumin demonstrates significant bioactivity in vivo, a phenomenon likely attributable to its accumulation in the intestines and subsequent modulation of systemic oxidative stress and inflammation. This article systematically reviews the comprehensive regulatory effects of curcumin on systemic metabolic networks—including glucose metabolism, amino acid metabolism, lipid metabolism, and mitochondrial metabolism—and explores their molecular basis, particularly how curcumin facilitates systemic metabolic improvements by alleviating oxidative stress and interacting with inflammation. Preclinical studies indicate that curcumin accumulates in the intestines, where it remodels the microbiota through prebiotic effects, enhances barrier integrity, and reduces endotoxin influx—all of which are critical drivers of systemic oxidative stress and inflammation. Consequently, curcumin improves insulin resistance, hyperglycemia, and dyslipidemia across multiple organs (liver, muscle, adipose) by activating antioxidant defense systems (e.g., Nrf2), enhancing mitochondrial respiratory function (via PGC-1α/AMPK), and suppressing pro-inflammatory pathways (e.g., NF-κB). Clinical trials have corroborated these effects, demonstrating that curcumin supplementation significantly enhances glycemic control, lipid profiles, adipokine levels, and markers of oxidative stress and inflammation in patients with obesity, type 2 diabetes, and non-alcoholic fatty liver disease. Therefore, curcumin emerges as a promising multi-target therapeutic agent against metabolic diseases through its systemic antioxidant and anti-inflammatory networks. Future research should prioritize addressing its bioavailability limitations and validating its efficacy through large-scale trials to translate this natural antioxidant into a precision medicine strategy for metabolic disorders.

Objective: To examine the influences and mechanisms of MicroRNA-19a-3p (miR-19a-3p) on endothelial dysfunction in atherosclerosis. Methods: An analysis of miR-19a expression was carried out using the Gene Expression Omnibus (GEO) database. The effect of miR-19a-3p on endothelial function in HUVECs was evaluated by miR-19a-3p overexpression under TNF-α treatment. Luciferase assays were performed to explore the potential target genes. Overexpression of junctional protein associated with coronary artery disease (JCAD) was used to examine the effects of miR-19a-3p on cell adhesion, and proliferation. Results: MiR-19a-3p expression in endothelial cells decreased after exposure to TNF-α and/or oscillatory flow, consistent with the expression change of miR-19a-3p found in atherosclerotic plaques. Additionally, endothelial cell dysfunction and inflammation were significantly diminished by miR-19a-3p overexpression but markedly exacerbated by miR-19a-3p inhibition. MiR-19a-3p transfection significantly decreased the expression of JCAD by binding to the 3’-UTR of JCAD mRNA. Furthermore, the protective effect of miR-19a-3p against endothelial cell dysfunction and inflammation was achieved by regulating JCAD and was closely linked to the Hippo/YAP signaling pathway. Conclusion: MiR-19a-3p expression is a crucial molecular switch in the onset of atherosclerosis and miR-19a-3p overexpression is a possible pharmacological therapeutic strategy for reversing the development of atherosclerosis.