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Force transduction at cell-cell adhesions regulates tissue development, maintenance and adaptation. We developed computational and experimental approaches to quantify, with both sub-cellular and multi-cellular resolution, the dynamics of force transmission in cell clusters. Applying this technology to spontaneously-forming adherent epithelial cell clusters, we found that basal force fluctuations were coupled to E-cadherin localization at the level of individual cell-cell junctions. At the multi-cellular scale, cell-cell force exchange depended on the cell position within a cluster, and was adaptive to reconfigurations due to cell divisions or positional rearrangements. Importantly, force transmission through a cell required coordinated modulation of cell-matrix adhesion and actomyosin contractility in the cell and its neighbors. These data provide insights into mechanisms that could control mechanical stress homeostasis in dynamic epithelial tissues, and highlight our methods as a resource for the study of mechanotransduction in cell-cell adhesions. The intestines, liver, and skin are all examples of organs that perform specific functions. Organs are comprised of tissues, which are themselves made up of cells. Epithelial tissue is one of the four basic types of tissue found in animals, and it occurs in almost every organ in the body. For example, epithelial tissue makes up the outermost layer of the skin, and the lining of the lungs and the intestines; the cells in epithelial tissues are attached to one another via ‘adhesion molecules’. Organs and tissues need to be maintained throughout life in order for them to work properly. Epithelial cells in particular are very short-lived and must be constantly replaced. If epithelial tissue is cut or damaged in any way, the surrounding healthy epithelial cells must work together to repair the wound and restore the tissue's integrity. These processes require individual epithelial cells to communicate with one another. While chemical signals provide one means of cell-to-cell communication, cells also sense and respond to the physical presence of surrounding cells. In adults, organs and tissues generally do not change shape or size; as such there is a tightly balanced exchange of mechanical forces between the individual cells. Damage to the tissue causes a detectable change in these mechanical forces, which is sensed by nearby healthy epithelial cells and causes them to work towards healing the wound. While the importance of mechanical forces in maintaining tissue integrity is widely recognized, there were few tools to study these forces; this meant that mechanical communication through cell–cell adhesion sites was not well understood. Now Ng, Besser et al. describe the development and use of a new method for measuring and mapping the exchange of mechanical forces at cell–cell adhesion sites. Changes in the strength of the forces exchanged between cells could be measured across clusters of multiple cells or for specific parts of individual cells. Ng, Besser et al. found that when an epithelial cell in a cluster started to divide to form two new cells, the cell exerted less mechanical force on its neighboring cells. Ng, Besser et al. found that the forces exerted between cells were strongest when there was more of an adhesion molecule called E-cadherin in the cell surface membrane at the cell–cell adhesion sites. The opposite was also true, as these forces were weakest at cell–cell adhesion sites with fewer E-cadherin molecules. The new method and findings will now help to guide future studies into how mechanical forces are transmitted between living cells.

In response to the hazards of icing in the energy, transportation, and aerospace sectors, extensive research has been conducted on anti‐icing materials based on the solid‐liquid/ice interface theory, as well as reliable chemical and electro‐thermal de‐icing systems. However, there is an urgent need for modernizing anti‐icing systems to address diverse application scenarios. Gaining insights into the influence of interface action forces on water droplet behavior can proactively prevent detrimental icing occurrences. Nevertheless, under severe conditions where ice formation is inevitable, leveraging interface action forces to induce cracking and expansion of ice facilitates its rapid detachment despite potential challenges associated with complete removal. A comprehensive review elucidating the mechanisms through which interface action forces impact water/ice formations encompasses various approaches toward designing mechanically‐driven de‐icing systems. As ‘energy‐free’ passive anti‐icing strategies have not yet been effectively implemented, a comprehensive understanding of the mechanisms through which mechanical forces influence the evolution of solid‐liquid, solid‐liquid/ice interfaces, and solid‐ice interfaces, as well as the integration of mechanical forces with various types of active/passive anti‐icing methods, can facilitate efficient de‐icing with minimal energy consumption. However, there still remains a potential challenge in completely removing water droplets/ice layers.

Mechanical damage is one of the predisposing factors of inflammation, and it runs through the entire inflammatory pathological process. Repeated or persistent damaging mechanical irritation leads to chronic inflammatory diseases. The mechanism of how mechanical forces induce inflammation is not fully understood. Piezo1 is a newly discovered mechanically sensitive ion channel. The Piezo1 channel opens in response to mechanical stimuli, transducing mechanical signals into an inflammatory cascade in the cell leading to tissue inflammation. A large amount of evidence shows that Piezo1 plays a vital role in the occurrence and progression of chronic inflammatory diseases. This mini-review briefly presents new evidence that Piezo1 responds to different mechanical stresses to trigger inflammation in various tissues. The discovery of Piezo1 provides new insights for the treatment of chronic inflammatory diseases related to mechanical stress. Inhibiting the transduction of damaging mechanical signals into inflammatory signals can inhibit inflammation and improve the outcome of inflammation at an early stage. The pharmacology of Piezo1 has shown bright prospects. The development of tissue-specific Piezo1 drugs for clinical use may be a new target for treating chronic inflammation.

Macrophages are the most important innate immune cells in humans. They are almost ubiquitous in peripheral tissues with a large variety of different mechanical milieus. Therefore, it is not inconceivable that mechanical stimuli have effects on macrophages. Emerging as key molecular detectors of mechanical stress, the function of Piezo channels in macrophages is becoming attractive. In this review, we addressed the architecture, activation mechanisms, biological functions, and pharmacological regulation of the Piezo1 channel and review the research advancements in functions of Piezo1 channels in macrophages and macrophage-mediated inflammatory diseases as well as the potential mechanisms involved.

Tumors often exhibit greater stiffness compared to normal tissues, primarily due to increased deposition within the tumor stroma. Collagen, proteoglycans, laminin, and fibronectin are key components of the extracellular matrix (ECM), interacting to facilitate ECM assembly. Enhanced fiber density and cross-linking within the ECM result in elevated matrix stiffness and interstitial fluid pressure, subjecting tumors to significant physical stress during growth. This mechanical stress is transduced intracellularly via integrins, the Rho signaling pathway, and the Hippo signaling pathway, thereby promoting tumor invasion. Additionally, mechanical pressure fosters glycolysis in tumor cells, boosting energy production to support metastasis. Mechanical cues also regulate macrophage polarization, maintaining an inflammatory microenvironment conducive to tumor survival. In summary, mechanical signals within tumors play a crucial role in tumor growth and invasion. Understanding these signals and their involvement in tumor progression is essential for advancing our knowledge of tumor biology and enhancing therapeutic approaches.

Hypertrophic scarring (HTS) is a major source of morbidity after cutaneous injury. Recent studies indicate that mechanical force significantly impacts wound healing and skin regeneration which opens up a new direction to combat scarring. Hence, a thorough understanding of the underlying mechanisms is essential in the development of efficacious scar therapeutics. This review provides an overview of the current understanding of the mechanotransduction signaling pathways in scar formation and some strategies that offload mechanical forces in the wounded region for scar prevention and treatment.

Cell geometry has long been proposed to play a key role in the orientation of symmetric cell division planes. In particular, the recently proposed Besson–Dumais rule generalizes Errera’s rule and predicts that cells divide along one of the local minima of plane area. However, this rule has been tested only on tissues with rather local spherical shape and homogeneous growth. Here, we tested the application of the Besson–Dumais rule to the divisions occurring in the Arabidopsis shoot apex, which contains domains with anisotropic curvature and differential growth. We found that the Besson–Dumais rule works well in the central part of the apex, but fails to account for cell division planes in the saddle-shaped boundary region. Because curvature anisotropy and differential growth prescribe directional tensile stress in that region, we tested the putative contribution of anisotropic stress fields to cell division plane orientation at the shoot apex. To do so, we compared two division rules: geometrical (new plane along the shortest path) and mechanical (new plane along maximal tension). The mechanical division rule reproduced the enrichment of long planes observed in the boundary region. Experimental perturbation of mechanical stress pattern further supported a contribution of anisotropic tensile stress in division plane orientation. Importantly, simulations of tissues growing in an isotropic stress field, and dividing along maximal tension, provided division plane distributions comparable to those obtained with the geometrical rule. We thus propose that division plane orientation by tensile stress offers a general rule for symmetric cell division in plants.

Bronchial asthma is a chronic inflammatory disease in which bronchial wall remodelling plays a significant role. This phenomenon is related to enhanced proliferation of airway smooth muscle cells, elevated extracellular matrix protein secretion and an increased number of myofibroblasts. Phenotypic fibroblast-to-myofibroblast transition represents one of the primary mechanisms by which myofibroblasts arise in fibrotic lung tissue. Fibroblast-to-myofibroblast transition requires a combination of several types of factors, the most important of which are divided into humoural and mechanical factors, as well as certain extracellular matrix proteins. Despite intensive research on the nature of this process, its underlying mechanisms during bronchial airway wall remodelling in asthma are not yet fully clarified. This review focuses on what is known about the nature of fibroblast-to-myofibroblast transition in asthma. We aim to consider possible mechanisms and conditions that may play an important role in fibroblast-to-myofibroblast transition but have not yet been discussed in this context. Recent studies have shown that some inherent and previously undescribed features of fibroblasts can also play a significant role in fibroblast-to-myofibroblast transition. Differences observed between asthmatic and non-asthmatic bronchial fibroblasts (e.g., response to transforming growth factor β, cell shape, elasticity, and protein expression profile) may have a crucial influence on this phenomenon. An accurate understanding and recognition of all factors affecting fibroblast-to-myofibroblast transition might provide an opportunity to discover efficient methods of counteracting this phenomenon.

Metastasis is a complicated, multistep process that is responsible for over 90% of cancer-related death. Metastatic disease or the movement of cancer cells from one site to another requires dramatic remodeling of the cytoskeleton. The regulation of cancer cell migration is determined not only by biochemical factors in the microenvironment but also by the biomechanical contextual information provided by the extracellular matrix (ECM). The responses of the cytoskeleton to chemical signals are well characterized and understood. However, the mechanisms of response to mechanical signals in the form of externally applied force and forces generated by the ECM are still poorly understood. Furthermore, understanding the way cellular mechanosensors interact with the physical properties of the microenvironment and transmit the signals to activate the cytoskeletal movements may help identify an effective strategy for the treatment of cancer. Here, we will discuss the role of tumor microenvironment during cancer metastasis and how physical forces remodel the cytoskeleton through mechanosensing and transduction.

Hematopoietic stem cells (HSCs) perceive both soluble signals and biomechanical inputs from their microenvironment and cells themselves. Emerging as critical regulators of the blood program, biomechanical cues such as extracellular matrix stiffness, fluid mechanical stress, confined adhesiveness, and cell-intrinsic forces modulate multiple capacities of HSCs through mechanotransduction. In recent years, research has furthered the scientific community’s perception of mechano-based signaling networks in the regulation of several cellular processes. However, the underlying molecular details of the biomechanical regulatory paradigm in HSCs remain poorly elucidated and researchers are still lacking in the ability to produce bona fide HSCs ex vivo for clinical use. This review presents an overview of the mechanical control of both embryonic and adult HSCs, discusses some recent insights into the mechanisms of mechanosensing and mechanotransduction, and highlights the application of mechanical cues aiming at HSC expansion or differentiation.