**1. Introduction**

Cells are neither amorphous blobs nor rigid, unchanging structures. They are able to sense, react and most of the time recover from many types of physical insults ranging from pores

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

created by osmotic shock or bacterial toxins to mechanical damages of various origins and intensity. Whatever the origin, the loss of barrier function provided by the plasmalemma leads to many potentially harmful effects including, but not limited to, the loss of intracellular content, the uncontrolled entry of Ca2+ and exposure of the intracellular milieu to reactive oxygen species (ROS), all of which may lead to a broad range of diminished cellular function, or even cell death. The negative effects of cellular injury are not limited to biochemical processes, they also directly affect the cell's structural integrity. As such, single-cell repair is as much a return to normal cell function as it is a return to structural integrity.

While they share common general steps of wound stabilization, resealing of plasmalemma damage and cytoskeletal remodeling, wound-healing mechanisms have been shown to vary widely according to the types of injury and cell-types. This chapter, using ubiquitous and injury- and cell-specific examples, aims to present an overview of the different mechanisms proposed for wound healing. Particular focus is put on how mechanotransduction, tension and tensegrity influences single-cell wound healing.
