Extracellular matrix (ECM)	ECM is a three-dimensional structure that encapsulates cells and defines their microenvironment, providing a physical scaffolding for the cellular constituents. ECM is a dynamic structure, constantly undergoing a remodeling process whereby ECM components are deposited, degraded, or modified. ECM dynamics are essential during restructuring of tissue architecture.
Integrins	A family of cell adhesion receptors that mediate either cell–cell interactions or cell–ECM interactions. Integrins are heterodimers with two distinct subunits, the α-subunit and the β-subunit.
Fibroblasts	The major cells responsible for the production of collagens, glycosaminoglycans, and proteoglycans, which are major components of the ECM.
Myofibroblasts	Specialized cells with both fibroblasts’ and SMCs’ phenotypic characteristics. These cells are activated by inflammatory cytokines and are involved in wound-healing mechanisms and in pathological conditions, such as fibrosis and chronic inflammation. They peculiarly express the α-SMA that they organize into the cytoskeleton to generate contractile force and migrate.
Fibroblast-to-myofibroblast transition	Phenotypic conversion of fibroblast into myofibroblast by transdifferentiation mechanisms occurring during wound healing, fibrosis, and inflammation. A well-characterized hallmark of the fibroblast-to myofibroblast transition is the novo formation of α-SMA stress fibers.
Focal adhesions	Transmembrane anchorage sites organized on the lower surface of the cell and in the cell’s periphery to anchor the underlying ECM fibrils. These structures are associated with the end of actin stress fibers and usually contain the αvβ3 integrin that interacts with a complex pattern of proteins including vinculin, talin, paxillin, α-actinin, zyxin, p125FAK, ILK, and other phosphotyrosine proteins and kinases.
Fibrillar adhesions	Integrin-containing complexes arising from focal adhesions, distributed on the upper cell surface, involved in the ECM fibrils’ organization. These elongated structures are enriched in α5β1 integrins bound to tensin.
Anoikis	Mechanism of programmed cell death or apoptosis induced by the loss of cell-ECM adhesion. Consequently, the ECM can be considered a survival signal for cells.
Cross-talk mechanism	Mechanism by which two or more surface receptors or two or more interactors recruited in different signal-transduction pathways affect each other and reinforce the downstream cell response to an extracellular signal.
Damage-associated molecular patterns (DAMPs)	Molecules released from damaged tissues, such as components or fragments of the ECM, released downstream of the cell injury. These danger signals bind specific receptors, such as Toll-like receptors, to elicit an immune response following tissue injury or in response to the changes in tissue composition and organization. DAMPs can also play a role in chronic pain conditions.
Tissue homeostasis	A homeostatic process involved in the maintenance of an internal steady state within a defined tissue of an organism, including control of cellular proliferation and death and control of metabolic function.
Redox homeostasis	Balance between intracellular reactive oxygen species (ROS) generation and elimination.