This mini-review discusses the cellular mechanisms underlying wound contraction, focusing on fibroblasts and myofibroblasts. It begins with a historical account of wound contraction in ancient Greek medicine, followed by a description of the three processes involved in wound closure: epithelization, connective tissue deposition, and contraction. The review explains that in mammals with loose skin, contraction leads to minimal scarring, while in humans, it can cause significant scarring or loss of function. The distinction between normal contraction and pathological contracture is made. The review highlights the role of fibroblasts in wound healing, which become activated after injury and migrate to the wound site, proliferate, and synthesize a new collagen-containing matrix called granulation tissue. Myofibroblasts, which are derived from fibroblasts, are responsible for generating the force necessary for wound contraction. These cells express α-smooth muscle actin and form tight adhesions to the surrounding tissue. The review also discusses in vitro models of wound contraction using fibroblasts cultured in collagen or fibrin matrices. It describes three common variations of the collagen matrix contraction model: floating matrix contraction, anchored matrix contraction, and stress relaxation. The differences in mechanical features between these models are discussed, with floating matrices resulting in a mechanically relaxed tissue and anchored matrices in a stressed tissue. The review explores the factors that regulate fibroblast contractility, including extracellular factors such as serum, transforming growth factor β (TGF-β), and platelet-derived growth factor (PDGF). It also discusses the differences in cell proliferation and collagen biosynthesis between fibroblasts in floating and anchored collagen matrices. The review concludes with a discussion of stress relaxation, which represents the transition from granulation tissue to dermis or scar, and the signaling mechanisms involved in this process. The findings suggest that mechanical organization of the tissue can regulate extracellular matrix biosynthesis and remodeling as well as cell proliferation.This mini-review discusses the cellular mechanisms underlying wound contraction, focusing on fibroblasts and myofibroblasts. It begins with a historical account of wound contraction in ancient Greek medicine, followed by a description of the three processes involved in wound closure: epithelization, connective tissue deposition, and contraction. The review explains that in mammals with loose skin, contraction leads to minimal scarring, while in humans, it can cause significant scarring or loss of function. The distinction between normal contraction and pathological contracture is made. The review highlights the role of fibroblasts in wound healing, which become activated after injury and migrate to the wound site, proliferate, and synthesize a new collagen-containing matrix called granulation tissue. Myofibroblasts, which are derived from fibroblasts, are responsible for generating the force necessary for wound contraction. These cells express α-smooth muscle actin and form tight adhesions to the surrounding tissue. The review also discusses in vitro models of wound contraction using fibroblasts cultured in collagen or fibrin matrices. It describes three common variations of the collagen matrix contraction model: floating matrix contraction, anchored matrix contraction, and stress relaxation. The differences in mechanical features between these models are discussed, with floating matrices resulting in a mechanically relaxed tissue and anchored matrices in a stressed tissue. The review explores the factors that regulate fibroblast contractility, including extracellular factors such as serum, transforming growth factor β (TGF-β), and platelet-derived growth factor (PDGF). It also discusses the differences in cell proliferation and collagen biosynthesis between fibroblasts in floating and anchored collagen matrices. The review concludes with a discussion of stress relaxation, which represents the transition from granulation tissue to dermis or scar, and the signaling mechanisms involved in this process. The findings suggest that mechanical organization of the tissue can regulate extracellular matrix biosynthesis and remodeling as well as cell proliferation.