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Cellulose fiber (CF) paper is a low-cost, sustainable, and flexible substrate, which has gained increasing interest recently. Before practical usage, the functionalization of the pristine CF paper is indispensable to meet requirements of specific applications. Different from conventional surface modification or physical mixing methods, we report in situ growth of ultralong hydroxyapatite nanowires (HAPNWs) with lengths larger than 10 μm on the CF paper. HAPNWs are radially aligned on the surface of CFs, creating a micro/nanoscale hierarchical structure. By means of the excellent ion exchange ability of HAP and the hierarchical structure, the functions of the CF paper can be easily customized. As a proof-of-concept, we demonstrate two kinds of functional CF paper: (1) the photoluminescent CF paper by doping Eu3+ and Tb3+ ions into the crystal lattice of HAPNWs and (2) the superhydrophobic CF paper by coating poly­(dimethylsiloxane) on the HAPNW hierarchical structure, which can be applied for self-cleaning and oil/water separation. It is expected that an in situ growth of ultralong HAPNWs will provide an instructive guideline for designing a CF paper with specific functions.

Pressure-overloaded left ventricular remodeling in young population is progressive and readily degenerate into heart failure. The aims of this study were to identify a plasma metabolite that predicts and is mechanistically linked to the disease. Untargeted metabolomics determined elevated plasma kynurenine (Kyn) in both the patient cohorts and the mice model, which was correlated with remodeling parameters. In vitro and in vivo evidence, combined with single-nucleus RNA sequencing (snRNA-seq), demonstrated that Kyn affected both cardiomyocytes and cardiac fibroblasts by activating aryl hydrocarbon receptors (AHR) to up-regulate hypertrophy- and fibrosis-related genes. Shotgun metagenomics and fecal microbiota transplantation revealed the existence of the altered gut microbiota-Kyn relationship. Supplementation of selected microbes reconstructed the gut microbiota, reduced plasma Kyn, and alleviated ventricular remodeling. Our data collectively discovered a gut microbiota–derived metabolite to activate AHR and its gene targets in remodeling young heart, a process that could be prevented by specific gut microbiota modulation.

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