1. ISG15 is highly expressed in both DKD mice and renal tubular epithelial cell cultured in HG condition.

2. ISG15 promotes DKD pyroptosis via NLRP3–CASP1–GSDMD axis.

3. ISG15–mtDNA–STING emerges as a critical hub that integrates the processes of pyroptosis

• In ageing fibroblasts, p16^INK4a concurrently enhanced STAT3 di-methylation mediated by EZH2 and suppressed the assembly of Bmi-1-EZH2/BCL-6 complexes at the NLRP3 promoter region.
• These dual regulatory actions synergistically upregulated STAT3-dependent NLRP3 transcription, thereby exacerbating inflammageing-driven ventricular remodelling following myocardial infarction.
• FNLM-nanocaged p16^INK4a-siRNA prevents post-infarction ventricular remodelling through inhibiting NLRP3 transcription in targeted cardiac fibroblasts.

ACT001 disrupts the MDK/c-Myc complex, enhancing c-Myc ubiquitination and overcoming temozolomide resistance in glioma. Combining ACT001 with temozolomide synergistically inhibits tumour growth and progression, offering a promising therapeutic strategy for glioma patients, particularly those with high MDK expression.

Ddr2 promotes PI3K/Akt/mTOR mediated autophagy inhibition, which contributes to Ang II-induced AF phenotypic switch.

1. NETs suppress the expression of MIR503HG by inducing promoter DNA methylation.
2. C/EBPβ binds to the NLRP3 promoter to promote NLRP3 expression.
3. MIR503HG inhibits the expression of C/EBPβ protein by promoting the interaction between C/EBPβ and the E3 ubiquitin ligase RNF43, thereby repressing NLRP3 expression.

With extended lifespans causing population aging, bone aging has become a worldwide issue. Cellular senescence in the bone microenvironment causes bone degeneration and dysfunction. This review summarises targets in cellular senescence and bone aging while detailing potential therapeutic strategies, including novel medicines and innovative biomedical materials. https://BioRender.com/0wqyt7g

1. MLKL plays a significant role in regulating endosomal transport of HSV-1 to nucleus during early stages of infection.
2. Formation of p-MLKL bodies during HSV-1 infection leads to death of oligodendrocyte and subsequent demyelination.
3. OPTN can negatively modulate MLKL levels to restrict infection and consequential oligodendrocyte death during HSV-1 infection.

Neutrophil extracellular traps are intricately linked to the tumor microenvironment and play a crucial role in tumorigenesis, metastasis, and related complications. Consequently, NETs-based tumor biomarkers and therapeutic strategies warrant significant attention.

Summary of key events initiated from Stress Zone and related cell populations in puncture-induced IVD degeneration.

Under hypoxic conditions, elevated PGK1 interacts with MYH9, promoting the ubiquitination and degradation of GSK3β, which leads to β-catenin stabilisation and nuclear translocation. Activated β-catenin increases the transcription of c-Myc and downstream targets genes enhancing cancer stemness, epithelial-to-mesenchymal transition (EMT), metastasis, and ESCC recurrence.

• Perlecan, a crucial component of basement membranes that plays a vital role in stabilising BSCB homeostasis and functions, was found to be upregulated in M2-sEVs.
• M2-sEVs decorated with RGD peptide can effectively target the neovascular endothelium surfaces at the injured spinal cord site.
• RGD-M2-sEVs promote BSCB restoration by transporting perlecan to neovascular endothelial cells, representing a potential strategy for SCI treatment.

1. OXA1L gene bi-allelic variants cause mitochondrial myopathy.
2. OXA1L deficiency results in combined mitochondrial respiratory chain defects and OXPHOS impairments.
3. OXA1L deficiency leads to elevated ROS production, which may activate the NF-κB signalling pathway, disturbing myogenic gene expression and triggering cell apoptosis.