Fort et al. identify a mechanobiological gate controlling mesoderm identity in human pluripotent stem cells. They show that actomyosin contractility suppre

Alzheimer’s disease (AD) is usually framed as a proteinopathy and network disorder, but this view may be incomplete. We propose a mechanobiological hypothesi...

Ocular nanomedicines for precise targeted delivery and controlled release in clinical application have expanded. However, developing materials that harmonize with biomechanical properties of various a...

3D-printed breast tissue models pave the way for cutting-edge lactation research.

In brief, Fan et al. develop a programmable-bacteria-macrophage system in which ultrasound (US)-triggered thermal stimulation induces bacterial lysis and therapeutic payload release. This process promotes macrophage repolarization toward the CD86-expressing phenotype within the tumor microenvironment, enhances immune cell infiltration, and highlights the role of tumor-cell mechanobiological properties in immunotherapy.

Aging leads to a progressive loss of muscle mass and strength, termed sarcopenia, which is accelerated by inactivity and exacerbated by intrinsic cellular and molecular dysfunctions within the musc...

Nature Nanotechnology, Published online: 11 June 2026; doi:10.1038/s41565-026-02179-0The Perspective highlights key challenges in mechanobiology, including the need to engineer multicellular reference models, develop and refine biophysical methods to manipulate and quantify biomechanical properties across scales and establish theoretical frameworks to interpret complex mechanobiological phenomena.

Read the full paper: Programmable-bacteria-macrophage backpacks for enhanced solid tumor therapy via mechanobiological interplay

Read the full paper: Mechanobiological antagonism of integrin β1/β3 gates YAP-driven reactionary dentinogenesis through fluid shear stress sensing

Read the full paper: Biomechanical Phenotyping Reveals Unique Mechanobiological Signatures of Early‐Onset Colorectal Cancer

Background Collective migration is the coordinated movement of a group of cells—a fundamental process in health and disease. Many models have been developed to study the molecular and physical mechanisms of collective migration. However, the aim of this study is to engineer a flexible in vitro framework that allows for mechanobiological quantification of the separate and combined contributions of individual cell mechanics to the directed migration of a collective. We utilised this framework to understand the role of juxtacrine Notch signalling during collective endothelial migration—an essential process during the formation of new blood vessels (known as angiogenesis). Results This framework enables users to perform high spatiotemporal analysis of migrative behaviour, cell–matrix traction forces, and intercellular forces in different microenvironments. With this framework, we show that Notch inhibited collectives adopt a distinct regime of directed collective migration. Whereas the directionality of migration, traction forces and intercellular forces are not affected by Notch inhibition, we observed spatiotemporal differences in migration speed, traction force magnitude and normal and shear stresses within Notch-inhibited collectives. Conclusions The in vitro framework is a powerful approach for dissecting the mechanisms of collective migration. With this framework, we show that a potential link exists between the juxtacrine signalling of Notch and an increased mechanical cohesiveness among collective cells.