R. Xu, F. Feng, X. Yu, Z. Liu, and L. Lao, "LncRNA SNHG4 Promotes Tumour Growth by Sponging miR-224-3p and Predicts Poor Survival and Recurrence in Human Osteosarcoma," Cell Proliferation 51, no. 6 (2018): e12515, https://doi.org/10.1111/cpr.12515. The above article, published online on 28 August 2018 in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, Qi Zhou; and John Wiley & Sons Ltd. Concerns were raised by a third party regarding duplicated images in multiple figures. An investigation by the publisher found apparent duplications within Figures3C and 5B, as well as images reused in or taken from other articles by different authors: 2E in Li etal. 2016 (https://doi.org/10.2147/JPR.S118581) and Guo etal. 2019 (https://doi.org/10.1155/2019/4390839); 5F in Zhang etal. 2018 (https://doi.org/10.1590/1414-431X20187439) and Zhu etal. 2019 (https://doi.org/10.18632/aging.102600); and 5B in Chen etal. 2019 (https://doi.org/10.1177/205873841882074) and Zhang etal. 2019 (https://doi.org/10.1007/s10120-019-01018-7). Due to the extent of these apparent duplications, the editor has lost confidence in the results reported, and therefore the article must be retracted. Corresponding author Lifeng Lao agrees with this decision. The other authors did not respond to the publisher's notice of retraction.

Osteocytes, the central regulators of bone remodelling, are essential for maintaining bone homeostasis. Embedded in a nutrient-limited matrix and burdened by cumulative stress over their exceptionally long lifespan, how osteocytes sustain long-term viability remains elusive. Tunnelling nanotubes (TNTs) are newly described intercellular bridges that enable long-range transfer of organelles and have been implicated in stress adaptation. Here, we provide the first definitive identification of TNTs between cultured osteocytes, which exhibit canonical TNT morphology together with osteocyte-specific features. Functionally, osteocytic TNTs mediate intercellular transfer of membrane-bound cargo, predominantly lysosomes. Under nutrient deprivation, TNT formation and lysosome transfer are both increased, replenishing the lysosomal pool in stressed osteocytes. Transferred lysosomes then fuse with accumulated autophagosomes, thereby restoring impaired autophagic flux and suppressing apoptosis. This cytoprotective effect requires TNT integrity and intact autophagic flux. Although mitochondrial transfer is detectable, it does not confer comparable protection. The findings identify a transcellular autophagy pathway mediated by TNT-dependent lysosome sharing, revealing a previously unrecognized cooperative survival strategy among osteocytes. This work establishes a novel conceptual framework in osteocyte biology and suggests potential therapeutic avenues for bone diseases associated with osteocyte apoptosis and impaired bone remodelling.

Alveolar bone injury represents a prevalent clinical challenge in dentistry, for which stem cell-based therapy has emerged as a promising strategy to promote bone regeneration. N-acetylcysteine (NAC), a potent antioxidant, has been shown to modulate the PI3K-AKT signalling pathway and potentially enhance osteogenesis; however, the specific downstream effectors mediating this process remain unidentified. In this study, post-extraction serum metabolomic profiling revealed that alveolar bone injury is accompanied by systemic oxidative stress and metabolic remodelling. Transcriptomic analysis of antioxidant-treated dental stem cells further identified type VI collagen A1 (COL6A1) as a key functional mediator. We subsequently investigated the role of COL6A1 in antioxidant-mediated osteogenesis through immunofluorescence and protein assays, and performed knockdown and invivo experiments to evaluate its function in oxidative stress regulation and osteogenic differentiation. Our results demonstrated that alveolar bone injury is associated with systemic oxidative stress and global metabolic alterations. Invitro, NAC markedly promoted the osteogenic differentiation of dental follicle stem cells (DFSCs) by activating the PI3K-AKT pathway and upregulating COL6A1. COL6A1 knockdown resulted in elevated reactive oxygen species (ROS) levels, impaired mitochondrial function, and attenuated NAC-mediated osteogenesis. Invivo, NAC-treated DFSCs exhibited enhanced bone healing and extracellular matrix (ECM) deposition in a rat model of alveolar bone injury, effects that were mediated through COL6A1 upregulation. Collectively, these findings demonstrate that NAC enhances osteogenesis in DFSCs via the PI3K-AKT-COL6A1 axis, offering a promising antioxidant-based strategy for stem cell therapies in bone regeneration. Moreover, COL6A1 is essential for maintaining redox homeostasis and represents a potential therapeutic target for improving regenerative outcomes.

Fatty acid (FA) overload imposes substantial stress on hypothalamic neurons, whilst whether cortical input could improve metabolic resilience of hypothalamic neurons remains poorly understood. Here, we reconstructed human cortical-hypothalamic assembloids (CO-HTO assembloids) to investigate how cortical input modulates hypothalamic responses to FA. Our results revealed that FA could impair neuronal survival, α-MSH secretion, and electrophysiological activity in hypothalamic organoids (HTOs). Remarkably, fusion with cortical organoids (COs) could prevent FA-induced apoptosis and functional defects, preserve mitochondrial respiration, and reduce lipid accumulation in HTOs. Also, transcriptomic and functional analyses revealed that cortical input could activate PGC1α-dependent mitochondrial biogenesis. Furthermore, pharmacological PGC1α activation or glutamate treatment rescued the FA-induced defects in HTOs. Collectively, our findings uncovered a cortico-hypothalamic regulatory axis and found glutamate-driven PGC1α activation might maintain hypothalamic neuronal stability and improve resilience to metabolic stress. Our CO-HTO assembloids provided a promising platform to investigate complex inter-regional communications and related neurological and metabolic disorders.

of the functions of the NTRK2 receptor during lung injury and regeneration. Our recent work using both human organoid and mouse disease models highlights the non-conventional role of NTRK2 isoforms in regulating pulmonary vasculature and alveolar regeneration during bronchopulmonary dysplasia.

LMPt enters the cell mainly through caveolin-mediated endocytosis, and then fuses with endosomes and lysosomes to deliver MPt to mitochondria and the endoplasmic reticulum to induce mitophagy based on the fusion of lysosomes and mitochondria, and endoplasmic reticulum stress and subsequent apoptosis via the Bip-PERK-eIF2α-ATF4 axis to exert an anti-breast cancer effect.

Although Myo-Inositol/D-Chiro-Inositol (Ins) and berberine (BBR) have each shown beneficial effects in polycystic ovary syndrome (PCOS), their combined therapeutic potential has not been systematically evaluated. Here, we demonstrate that Ins/BBR exerts superior efficacy compared with single treatments by targeting multiple pathogenic pathways in PCOS. In a DHEA+HFD-induced mouse model, Ins/BBR restored systemic sex steroid balance, normalized LH/FSH ratio, and improved estrous cyclicity. It also reduced ovarian cysts and enhanced fertility, accompanied by partial normalization of steroidogenic enzyme expression. At the cellular level, Ins/BBR alleviated mitochondrial defects and broadly reprogrammed metabolic landscape in granulosa cells, in specific, restoring nucleotide pools and amino acid turnover and preventing abnormal long-chain fatty acid accumulation. Together, these findings provide preclinical evidence that Ins/BBR acts through coordinated endocrine, ovarian and metabolic mechanisms, supporting its promise as a safe and effective therapeutic strategy for PCOS.

Rutin directly binds to GSK3β, stabilising β-catenin and activating Wnt/β-catenin signalling to drive hair cycle.

ABSTRACTHigh altitude pulmonary hypertension (HAPH) is a complex disease featured by hypoxia‐induced pulmonary vasoconstriction and remodelling of small pulmonary arterioles, which could lead to increased pulmonary pressures and right ventricular hypertrophy and eventually result in heart failure. The temporal trajectory of HAPH progression can be divided into three overlapping phases: hypoxic pulmonary arterioles vasoconstriction, hypoxic pulmonary arterioles remodelling and even right heart failure. Each phase is governed by distinct molecular engines and cellular effectors that translate hypoxia physiological adaption into irreversible cardiopulmonary dysfunction. This review describes the intricate cellular signalling networks involved in the pathogenesis of HAPH, integrating canonical pathways such as HIF, MAPK and BMP with emerging targets like Wnt/β‐catenin, Notch, Hippo‐YAP and IL‐6. Inhibiting the HIF signalling pathway, modulating the MAPK pathway and suppressing the BMP, Wnt/β‐catenin, Notch, Hippo‐YAP and IL‐6 pathways have shown potential in reducing vascular remodelling and right ventricular dysfunction. Despite encouraging progress, the clinical translation remains constrained by a lack of deeper understanding of the signalling networks in HAPH. A comprehensive understanding of these signalling pathways in HAPH may yield critical insights into the disease's pathogenesis and facilitate the development of targeted intervention strategies. Future research should focus on elucidating the molecular mechanisms underlying these pathways, exploring genetic and environmental interactions, validating intervention targets, developing biomarkers, utilising systems biology approaches and conducting clinical trials.