Nature Nanotechnology, Published online: 29 September 2026; doi:10.1038/s41565-026-02280-4
Four-inch rhombohedral-stacked boron nitride wafers are reproducibly synthesized through a step-templated interfacial epitaxy strategy, exhibiting high-density, fast-speed and non-volatile memory performances.
Nature Nanotechnology, Published online: 08 September 2026; doi:10.1038/s41565-026-02262-6
Charge-switching S-lipids generate S-lipid nanoparticles that are neutral or negative at physiological pH but become cationic in acidic endosomes, enabling nucleic acid delivery with reduced inflammation compared with conventional LNPs.
Nature Cancer, Published online: 25 August 2026; doi:10.1038/s43018-026-01221-3
Chen and colleagues report that the neuropeptide galanin impairs antitumor immunity in glioblastoma by interacting with its receptor GALR3 on monocytic myeloid-derived suppressor cells, promoting their infiltration and ferroptosis resistance.
Chin Med J (Engl). 2026 May 19. doi: 10.1097/CM9.0000000000004098. Online ahead of print.
ABSTRACT
High-salt diet (HSD) has emerged as a prevalent environmental factor that exacerbates chronic inflammation and insulin resistance in obesity-associated type 2 diabetes (T2D) by modulating macrophage polarization, metabolic reprogramming, and epigenetic imprinting. Current evidence demonstrates that HSD activates p38/mitogen-activated protein kinase (MAPK), nuclear factor kappa-B (NF-κB), and NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome signaling pathways, by which it drives macrophage polarization toward a proinflammatory M1 phenotype while inducing a glycolysis-dominant metabolic shift, thereby establishing a persistent "metabolic memory". Moreover, HSD orchestrates metabolic memory in macrophages through coordinated epigenetic machinery, including histone modifications (Trimethylation of histone H3 at lysine 4 [H3K4me3] and Acetylation of histone H3 at lysine 27 [H3K27ac]), DNA methylation, and noncoding RNAs (e.g., long non-coding RNA MALAT1 and miR-155), leading to sustained inflammatory phenotypes. In multiple metabolic organs (e.g., adipose tissue, liver, pancreas, and gut), the HSD-macrophage axis aggravates systemic insulin resistance through shared proinflammatory signaling and other tissue-specific mechanisms. Most importantly, therapeutic strategies targeting the NLRP3 inflammasome, metabolic pathways, and epigenetic alterations offer novel approaches for managing metabolic inflammation. Future investigations are encouraged to leverage lineage tracing, single-cell sequencing, and spatial multi-omics technologies to advance the development of precision medicine for macrophage-associated metabolic disorders.
PMID:42156155 | DOI:10.1097/CM9.0000000000004098
Nature, Published online: 08 April 2026; doi:10.1038/s41586-026-10342-9
A clinical phase 1 trial of a single infusion of CS-101, CD34+ cells modified using a transformer base editor to reactivate fetal haemoglobin production, led to early and enduring transfusion independence in patients with β-thalassaemia.
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