The cover image is based on the article Intelligent Manufacturing for Osteoarthritis Organoids by Xukun Lyu et al., https://doi.org/10.1111/cpr.70043.

One-third of the world's population is affected by metabolic syndrome. Complicated pathogenesis and limited drugs cause the growing prevalence of metabolic syndrome. Macrophage-mediated metaflammation is closely associated with the development of metabolic syndrome. The role of phytochemicals targeting macrophages in the treatment of metabolic syndrome has received increasing attention.

This graphical abstract illustrates the reciprocal crosstalk between the brain and peripheral organs, highlighting the profound impact of exercise on brain health through systemic interactions. It underscores how exercise influences the brain via signals from various organs and, conversely, how the brain modulates functions of peripheral organs. This integrative perspective sheds light on the bidirectional communication that underpins the interplay between physical activity, brain function and systemic health.

Overall schematic of intelligent manufacturing in osteoarthritis organoids. Broad overview of the article's structure, outlining the progression from fundamental joint anatomy and OA pathogenesis to organoid construction and, ultimately, to intelligent manufacturing and future prospects.

Our results suggested that mitochondria-accelerated motile cilia intraflagellar transport may be involved in endometrial microenvironment establishment.

Illustration of the preparation of tFNAs-DJ-1 saRNAs complex and its inhibitory effects on ferroptosis in R28 and retina.

We speculated lack of Klotho (KL) would aggravate club cell senescence, which contributes to COPD inflammation. In this study, we collected chronic obstructive pulmonary disease (COPD) lung tissue using single-cell RNA sequencing (scRNA-seq), revealing club cell heterogeneity and cellular senescence in COPD. Club cells were divided into four subpopulations, in addition, KL and club cell secretory proteins (CCSP) were downregulated in cigarette smoke (CS)-induced COPD mice, associated with increasing age-related markers. After KL knockout, more ciliated cells appeared where club cells disappeared, and resulting CCSP downregulation. Furthermore, KL deficiency aggravated club cell senescence and CSE-induced pulmonary inflammation. To investigate the specific regulation mechanism, hnRNPA2/B1 was recognised and identified it was the key molecule in KL-regulated club cell senescence, and neddylation of club cell was a crucial factor contributing to hnRNPA2/B1 downregulation. Thus, we concluded that KL could regulate club cell senescence and differentiation. When CS stimulates the small airway epithelium, KL deficiency aggravates lung inflammation, club cell senescence and dysfunctional of ciliated cell. Targeting neddylation might be a promising strategy to reverse lung aging and club cell senescence. This study describes a novel mechanism about COPD-linked lung inflammation.

Under 3D suspension culture condition, the expandable hepatoblast organoids and mature polarised hepatocyte organoids were established by low concentration of Matrigel from human embryonic stem cells, which recapitulated the gene expression signatures and functions of primary human hepatoblast and hepatocytes. The dynamic culture system by using bioreactors further enlarged the scale of hepatocyte organoid culture.

Cardiomyocytes with high m.3243A>G burden exhibited hypertrophic phenotype. Mitochondria dysfunction occurred and tended to become round in cardiomyocytes with high m.3243A>G burden. Mitochondria-associated ER membrane (MAM) was disrupted in cardiomyocytes with high m.3243A>G burden. Mutation reduction and MAM enforcement partially reversed the cellular behaviour.

PDHA2, a testis-specific subunit of pyruvate dehydrogenase, is required for the conversion of pyruvate to acetyl-CoA. Its absence results in decreased acetyl-CoA and precursors for metabolites and energy during spermatogenesis. This results in decreased histone acetylation, defective chromosome structure and moderately reduced crossovers, ultimately leading to male infertility.

We optimised a protocol that combines developmental patterning with mechanical cut to produce pint-sized midbrain organoids, with diameters less than 300 μm, suitable for long-term evaluation, along with a comprehensive functional assay system consisting of calcium transient assay, neurite extension assay, and multielectrode array assay.

tRF-3a is the main tsRNA subtype up-regulated in HBV-related HCC. tRF-3a-Pro is significantly up-regulated in HBV-related HCC tumour than that in paratumour tissues. The level of tRF-3a-Pro in serum is a promising candidate biomarker for HCC diagnosis. tRF-3a-Pro promotes cell proliferation and regulates cell cycle of HCC.

Lung cancer development involves mechanisms like reduced EGFR/EGF ubiquitination driving cancer cell behaviors and immune evasion via loss of PD-1/PD-L1 ubiquitination. Balancing ubiquitination and deubiquitination may be a potential therapeutic strategy.

GANT61 induced autophagy via the AKT pathway and promoted the accumulation of lipid droplets in both cell lines. The molecular mechanism behind this lipid accumulation appears to involve the mediation of SREBP1. Furthermore, the combination of GANT61 with CQ/Fatostatin significantly inhibited the proliferation and clonogenicity of SKOV3 and SKOV3PTX cells.