•Brain-centric lncRNAs regulate gene networks, and their disruption is linked to MDD.

•In MDD, altered lncRNAs disrupt gene regulation by changing chromatin looping or modifying chromatin accessibility.

•These changes lead to neuronal dysfunction, affecting neural circuitry and synaptic plasticity.

•The result is impaired brain function, contributing to the symptoms of MDD.

•The BBB hinders mAb-based brain disorder therapies

•A brain-targeted B-cell-depleting mAb for MS that efficiently crosses the BBB via hTfR1 was developed using Brainshuttle^™ technology (1a and 1b)

•The Brainshuttle^™-CD20 mAb was well tolerated (2a and 2b) and displayed B-cell-killing properties (1c), paving the way for future development and clinical translation of TfR1-targetingtherapies for increased brain penetration

•MAFLD is associated with increased hepatocytes NRF2 expression.

•NRF2 alleviates MAFLD by suppressing pyroptosis.

•NRF2 directly inhibits GSDMD expression to regulate pyroptosis.

•Targeting the NRF2–pyroptosis (GSDMD) axis offers a potential therapeutic strategy for MAFLD.

•Irisin mediated muscle-kidney crosstalk mitigated tubular injury and inflammation.

•Irisin inhibited the cGAS-STING signalling activation via integrin αV/β5 in tubular epithelial cells.

•Irisin was a predictive biomarker and a promising candidate for CI-AKI.

•m5C modifications are dynamically regulated by writers, readers, and erasers, influencing cancer progression, metastasis, and immune evasion.

•Distinct m5C regulatory networks exist across cancers, modulating oncogenic pathways and therapy responses.

•m5C signatures serve as biomarkers for cancer prognosis and treatment stratification, highlighting their role in precision oncology.

•Pro-inflammatory cytokines are significantly upregulated in the synovial fluid T cells in rheumatoid arthritis patients.

•The expression of pro-inflammatory cytokine interferon-γ (IFN-γ) positively correlates with the high expression of inhibitor of differentiation 2 (Id2).

•The inhibition or ablation of Id2 can effectively suppress IFN-γ production and the onset and progression of arthritis.

•LINC02776 promotes OC cell proliferation by regulating DNA damage and apoptosis signaling pathways.

•LINC02776 binds PARP1 to promote DNA damage-triggered PARylation in OC cells.

•LINC02776 mediates cisplatin and olaparib resistance in OC cells by enhancing PARP1-mediated PARylation activity and regulating the PARP1-mediated HR pathway.

•The high expression of LINC02776 is induced by HIF-1α in platinum-resistant OC cells and tissues.

•Canonical Hippo pathway activated in nphp1-deficient disease models and patients.

•Kibra was a key upstream molecule in regulating the activation of canonical Hippo pathway in nphp1-deficient disease models and patients and closely related to renal cyst formation and fibrosis in nphp1^KO mice.

•Elevated SH3GL1 expression in DLBCL patients was associated with a negative prognosis.

•SH3GL1 plays a crucial role in promoting DLBCL cell survival through the regulation of FTH1-mediated ferroptosis and doxorubicin resistance.

•Zfp36 was initially demonstrated to attenuate cardiac hypertrophy through the inhibition of ferroptosis in cardiomyocytes, providing a new target for therapeutic strategies targeting ferroptosis.

•Zfp36 facilitated the degradation of Ythdc2 mRNA by binding to it, subsequently inhibiting Ythdc2-mediated degradation of SLC7A11 mRNA, and maintaining GSH levels. This elucidates a previously unrecognized regulatory pathway in the context of cardiac hypertrophy.

•Genome-wide profiling reveals the redistribution of m6A modification on pseudogene-derived lncRNAs and m6A redistribution-relevant dysregulation of pseudogenes in HGSOC.

•RPS15AP12, as a representative processed pseudogene, is up-regulated by FTO-mediated demethylation and acts as a miRNA sponge to promote RPS15A expression via competitively binding to miR-96-3p.

•RPS15AP12/RPS15A axis inhibits MAVS sensors (RIG-I and MDA5) and downstream IFN-β levels in ovarian cancer.

•ModRNAs-transfected hADSCs exhibit pulsed and transient expression, enabling efficient production of functional VEGFA and bFGF proteins.

•Intracardiac injection of these engineered hADSCs leads to the enhancement of cardiac function and the improvement of electrical conduction.

•The hADSCs^dual mainly exerts its effect on myocardial infarction by promoting stable vascular regeneration and suppressing cell apoptosis.

•TREM2 knockout worsens kidney injury and accelerates AKI–CKD transition.

•TREM2 is upregulated by hypoxia via HIF1α in AKI–CKD transition.

•An adoptive cell therapy using TREM2-overexpressing macrophages reduces kidney inflammation and fibrosis.

•Ferroptosis-related mechanisms significantly affect the biology of CD4⁺ T-cell subsets and are further involved in inflammatory diseases.

•Crosstalk between CD8⁺ T cells and tumour cells induces ferroptosis in the tumour microenvironment.

•Glutathione peroxidase 4 loss promotes regulatory T-cell ferroptosis to enhance anti-tumour immunity.

•CD39+ Tregs in peripheral blood are associated with poor response to anti-PD-1 immunotherapy in advanced breast cancer.

•Higher frequencies of CCR2+ monocyte-derived dendritic cells correlate with better immunotherapy outcomes.

•A predictive model based on CD39+ Tregs and monocyte-derived dendritic cells effectively distinguishes patient progression-free survival.

•Peripheral blood biomarkers offer a non-invasive approach to guide immunotherapy choices.

•Topical TYK2 inhibitor alleviates psoriasis-like dermatitis.

•Topical TYK2 inhibitor reduces psoriasis progression through restraining the inflammatory responses of keratinocytes.

•The inhibition of TYK2 regulates the inflammatory response of keratinocytes through AKT-SP1-NGFR-AP1 pathway.

•LINC01088 is transcriptionally upregulated by SP1.

•LINC01088 acts as a scaffold platform to bind USP7 and HLTF.

•USP7, as a deubiquitinating enzyme of HLTF, participates in inhibiting the ubiquitin-proteasome degradation of HLTF.

•HLTF transcriptionally upregates the expression of downstream SLC7A11, and ferroptosis of GBM cells was inhibited.

•Comparative analysis: Evaluation of organoids, animal models, and 2D models, highlighting their respective strengths and limitations in replicating physiological conditions and studying disease processes.

•Vascularisation techniques: Comparative evaluation of vascularised organoid fabrication methods, emphasising their efficiency, scalability and ability to replicate physiological vascular networks.

•Material selection: Thorough evaluation of materials for vascularised organoid culture system, focusing on those that effectively mimic the extracellular matrix and support vascular network formation.

•Applications: Overview of organoid applications in basic cancer research and clinical settings, with an emphasis on their potential in drug discovery, disease modelling and exploring complex biological processes.

•We preliminarily confirmed GI-Y2 as a novel inhibitor of GSDMD via structure-based virtual screening and pharmacological validation.

•GI-Y2 directly interacts with GSDMD and reduces the membrane binding of GSDMD-N via the Arg10 residue.

•GI-Y2 inhibits the formation of atherosclerotic plaques by targeting GSDMD and GI-Y2 reduces pyroptosis and macrophage infiltration in atherosclerosis.

•We constructed macrophage membrane-coated GI-Y2 nanoparticles to enhance the targeting of GI-Y2 to macrophages in atheromatous plaques and demonstrated its vascular protective effect in vivo.

•METTL14 controls osteoclast-mediated bone resorption by means of the methylation (4249 A) of the NFATc1 gene during osteoclast differentiation.

•Exon junction complexes (EJCs) protect the remaining methylation sites of the NFATc1 gene (located in the inner exon fragment of 50–200 nt) from hypermethylation and degradation.

•The “shield effect” disappears when the exon fragment is extended to 300 nt. Downstream, YTHDF2 induced the degradation of hypermethylation NFATc1 transcripts without site restriction.

•Study involved 427 women with HIV.

•Identified 245 aberrant DNA methylation sites and 85 methylation regions in CD4+ T cells linked to the HIV-1 reservoir.

•Highlighted genes are involved in viral replication, immune defence, and host genome integration.

•Findings suggest potential molecular targets for eradication strategies.

•YBX1 inhibits ferroptosis in HCC by regulating the RNF115-DHODH axis.

•RNF115, an E3 ligase, mediates K27 ubiquitination and autophagic degradation of DHODH.

•YBX1 binds to the m5C sites of RNF115 mRNA 3′-UTR and interacts with EIF4A1 to bridge the 5′-UTR, promoting mRNA circularisation and translation.

•High expression of YBX1/RNF115 predicts the poor overall survival in HCC.

•OTUD5 mediates GPX4 deubiquitination to regulate its stability.

•Deletion of OTUD5 promotes ferroptosis and inhibits tumor growth.

•Wild type p53 inhibits OTUD5 transcription, thereby promoting GPX4 degradation and inhibiting the development of gastric cancer.

•OTUD5, GPX4 expression and p53 activity are highly correlated and correlates with clinical progression in STAD.

•The role of citrullinization in cisplatin resistance of OSCC.

•PADI4 citrullinate of PRMT2 and stabilize PRMT2.

•PADI4 citrullinate of PRMT2 promoting the transcription of IDs family (ID1, ID2 and ID3) via histone arginine methylation.

•PADI4 citrullinated PRMT2 affected the combination of PRMT2 and USP7.

•PADI4 citrullinate of PRMT2 at R312 site.

•PADI4 inhibitor GSK484 can affect the stemness of OSCC and cisplatin resistance.

•Intratumoral Fusobacterium nucleatum exhibits significant spatial heterogeneity within breast cancer tissues.

•F. nucleatum colonization alters the expression of key proteins involved in tumour progression and migration.

•The MAPK signalling pathway is a critical mediator of F. nucleatum-induced breast cancer cell proliferation and migration.

•VEGFD and PAK1 are potential therapeutic targets to mitigate F. nucleatum-induced tumour progression.