NRF2 Hijack Creates Tumour-Friendly Macrophages
Journal: Nature (2025)
Author: Hegde, S., Giotti, B., Soong, B.Y. et al., USA / France
Tumours activate the NRF2 pathway in bone-marrow myeloid progenitors, silencing interferon signaling and pushing monocytes to become macrophages that dampen anti-tumour immunity. This early progenitor reprogramming creates a systemic immune shield that supports cancer growth. Blocking NRF2 restores interferon responses and enhances the efficacy of checkpoint immunotherapy, revealing a new target for combination cancer treatments.
Stem Cell Grafts Repair Stroke Through Molecular Crosstalk
Journal: Nat Commun 16, 8224 (2025)
Author: Weber, R.Z., Achón Buil, B., Rentsch, N.H. et al., Switzerland / USA
Human iPSC-derived neural progenitors transplanted into post-stroke mouse brains survive for months, integrate into host tissue, and differentiate into functional GABAergic neurons. The grafts reduce inflammation and secrete factors that rewire host circuits, promoting behavioral recovery. Molecular profiling shows a sustained dialogue between donor and host cells, highlighting a powerful regenerative strategy for ischemic brain injury.
Synthetic Matrix Guides Placental Organoids for Early-Stage Insights
Journal: Nat Commun 16, 8267 (2025).
Author: Richards, C., Chen, H., O’Rourke, M. et al., Australia
A custom PEG-based synthetic matrix enables precise bioprinting of trophoblast organoids that mimic early human placental development. The engineered environment biases cells toward extravillous trophoblast lineages, a key step in implantation and vascular remodeling. This reproducible model opens avenues for studying pregnancy disorders like preeclampsia and for screening therapeutics under controlled conditions.
Prion Identity Outweighs Host Genetics in Brain Organoids
Journal: npj Dement. 1, 25 (2025).
Author: Groveman, B.R., Foliaki, S.T., Williams, K. et al.. USA/ Italy
Human brain organoids, whether carrying familial mutation or not, faithfully propagate the distinct biochemical and seeding features of FFI or sporadic CJD prions after infection. The prion strain’s identity dominates over the genetic background of the host tissue, demonstrating that prion conformation drives disease phenotype. This platform provides a controlled system for studying prion mechanisms and testing candidate therapeutics.
