Methyl 3-chloroasterric acid exerted anti-neuroinflammatory and antidepressant effects through the downregulation of P2Y1R.

Stapled anoplin with perfluoroaryl-cysteine enhances antibacterial activity.

Metal exposure in heart disease.

Mechanism study on the inhibition of lactoferrin glycation and AGEs production by pineapple Peel polyphenols based on molecular interaction and antioxidant synergy.

Click chemistry synthesis of triazole-grafted quinazolinones as new multi-panel anticancer agents: mechanistic insights into apoptosis and cell cycle arrest in colorectal cancer.

Cryptotanshinone suppresses ESCC metastasis by inhibiting macrophage polarization: A mechanistic study elucidating the rationale for cisplatin combination.

Tailored covalent organic frameworks with tunable fluorine groups for efficient adsorption of bisphenol analogues.

New nonacyclic duclauxin derivatives with potent anti-influenza activities from Antarctic fungus Penicillium sp. CPCC 401065.

Aqueous zinc-ion batteries employing organic cathodes hold promise for grid-scale energy storage, yet they are frequently hindered by active material dissolution and slow reaction kinetics. Herein, we report a bipolar organic cathode, HATN-T, designed by integrating stable nitroxyl radicals into a conjugated hexaazatrinaphthylene (HATN) scaffold. This claw-shaped molecular design features multiple redox-active centers (C═O, C═N, and N-O•) to facilitate reversible multi-ion (Zn2+, H+, and ClO4 -) storage. As a cathode, HATN-T delivers a high specific capacity (316 mAh g-1 at 0.1 A g-1), exceptional rate performance (260 mAh g-1 at 10 A g-1), and robust cycling stability (79% retention after 5000 cycles). Mechanistic studies reveal that the charge storage is dominated by capacitance, originating from the synergistic redox activity of the integrated functional groups. Notably, the reversible formation of a zinc hydroxychloride byproduct acts as a chemical buffer, confirming a proton-coupled mechanism that underpins the electrode's exceptional reversibility. This work establishes a generalizable design strategy for merging stable radicals with conjugated scaffolds to create high-performance organic electrodes for sustainable energy storage.

Dimethyl fumarate attenuates post-infarct myocardial injury and is associated with modulation of the NRG-1/ErbB2/Akt pathway and reduction of oxidative stress.

SGLT2 inhibitors ameliorate myocardial hypertrophy in rats via AMPK/Nrf2-mediated ferroptosis suppression and antioxidant response.

Breaking the oncogene-immune suppression cycle through dual HER2 silencing and innate immune activation by biomineralized DNA nanocomplexes.

Design, synthesis and biological evaluation of testosterone derivatives as potential anti-tumor and anti-inflammatory agents.

Inflammatory bowel diseases (IBD), comprising Crohn's disease and ulcerative colitis, are chronic, relapsing inflammatory disorders increasingly recognized as systemic conditions with significant extraintestinal manifestations. Over the past 3 decades, the prevalence of IBD has risen in parallel with obesity and related metabolic disorders, including type 2 diabetes mellitus (T2DM), cardiovascular disease (CVD), chronic kidney disease (CKD), metabolic dysfunction-associated steatotic liver disease (MASLD), and dyslipidemia. This parallel rise raises the possibility of shared or interacting biological pathways linking metabolic dysfunction and intestinal inflammation. Epidemiologic studies suggest increased risks of metabolic comorbidities in IBD independent of traditional factors, while mechanistic insights implicate systemic meta-inflammation, mesenteric adipose tissue remodeling (creeping fat), gut barrier dysfunction, and altered lipid and glucose metabolism. These pathways perpetuate a cycle of immune dysregulation and metabolic injury, amplifying disease severity and complications. Obesity and insulin resistance further impact IBD outcomes by altering pharmacokinetics and therapeutic response to biologics, with a higher body mass index associated with increased treatment failure, earlier loss of response, and heightened infection risk. Emerging data also suggest potential dual benefits of metabolic-directed therapies, such as glucagon-like peptide-1 receptor agonists, which may improve weight, glycemic control, and inflammatory indices. However, most evidence remains observational, with limited longitudinal or mechanistic studies. This narrative review synthesizes current knowledge at the interface of IBD and metabolic dysfunction, highlighting clinical implications, translational insights, and research gaps. Integrating metabolic screening and multidisciplinary management into IBD care may improve outcomes, while future mechanistic and interventional studies are needed to define therapeutic strategies that address both gut inflammation and systemic metabolic disease.

Bergenin lipid prodrug nanoparticles: Synthesis, enhanced oral bioavailability, and mechanistic studies

BLM helicase deficiency impairs porcine oocyte maturation via induction of organelle dysfunction.

Structural studies of N, O donor (imino)/(amino)pyridine mononuclear zinc(II) complexes as catalysts in the ring-opening polymerization reactions of rac-lactide

METTL3-mediated m6A modification of circWDR85 drives breast cancer bone metastasis via the CKB/c-Jun axis.

Organic acidemias (OAs) are a group of inherited disorders, most commonly caused by defects in mitochondrial enzymes involved in amino acid and fatty acid metabolism. While they characteristically present with metabolic and neurological crises, growing evidence reveals a significant burden of chronic immune dysregulation in some disorders and patients. This review provides a synthesis of clinical and mechanistic evidence discussing immune dysregulation in OAs. Cytopenia can occur in OAs and predispose patients to recurrent and severe infections. Adaptive immune deficits, such as hypogammaglobulinemia, reduced B and T cell populations, and impaired vaccine-specific antibody responses, including to diphtheria and tetanus in MSUD and to the inactivated COVID-19 vaccine in propionic acidemia, have also been reported. Additionally, some case series note hyperinflammatory conditions, such as hemophagocytic lymphohistiocytosis. Mechanistic studies indicate that accumulated metabolites disrupt innate and adaptive hematopoietic progenitor function, mitochondrial homeostasis, and inflammatory signaling. Emerging therapeutic avenues, such as gene and mRNA-based therapies, hold the potential to improve or normalize the biochemical phenotype in OAs. While their impact on immune abnormalities remains largely unexplored, future clinical trials offer an opportunity to systematically assess potential effects on immune parameters. OAs are increasingly recognized as disorders with intrinsic immune dysregulation, extending beyond their well-characterized metabolic and neurological manifestations. Future clinical trials will benefit from including immunological endpoints to evaluate immunological recovery for novel therapies.

Integrative genomics elucidates the evolutionary, temporal, and developmental origins of a hydrocephalus risk gene.