Pericytes (formerly called Rouget cells) are multi-functional mural cells of the microcirculation that wrap around the endothelial cells that line the capillaries throughout the body. Pericytes are embedded in the basement membrane of blood capillaries, where they communicate with endothelial cells by means of both direct physical contact and paracrine signaling. The morphology, distribution, density and molecular fingerprints of pericytes vary between organs and vascular beds. Pericytes help in the maintainenance of homeostatic and hemostatic functions in the brain, where one of the organs is characterized with a higher pericyte coverage, and also sustain the blood–brain barrier. These cells are also a key component of the neurovascular unit, which includes endothelial cells, astrocytes, and neurons. Pericytes have been postulated to regulate capillary blood flow and the clearance and phagocytosis of cellular debris in vitro. Pericytes stabilize and monitor the maturation of endothelial cells by means of direct communication between the cell membrane as well as through paracrine signaling. A deficiency of pericytes in the central nervous system can cause increased permeability of the blood–brain barrier.

In the central nervous system (CNS), pericytes wrap around the endothelial cells that line the inside of the capillary. These two types of cells can be easily distinguished from one another based on the presence of the prominent round nucleus of the pericyte compared to the flat elongated nucleus of the endothelial cells. Pericytes also project finger-like extensions that wrap around the capillary wall, allowing the cells to regulate capillary blood flow.

Both pericytes and endothelial cells share a basement membrane where a variety of intercellular connections are made. Many types of integrin molecules facilitate communication between pericytes and endothelial cells separated by the basement membrane. Pericytes can also form direct connections with neighboring cells by forming peg and socket arrangements in which parts of the cells interlock, similar to the gears of a clock. At these interlocking sites, gap junctions can be formed, which allow the pericytes and neighboring cells to exchange ions and other small molecules. Important molecules in these intercellular connections include N-cadherin, fibronectin, connexin and various integrins.

In some regions of the basement membrane, adhesion plaques composed of fibronectin can be found. These plaques facilitate the connection of the basement membrane to the cytoskeletal structure composed of actin, and the plasma membrane of the pericytes and endothelial cells.

Pericytes in the skeletal striated muscle are of two distinct populations, each with its own role. The first pericyte subtype (Type-1) can differentiate into fat cells while the other (Type-2) into muscle cells. Type-1 characterized by negative expression for nestin (PDGFRβ+CD146+Nes-) and type-2 characterized by positive expression for nestin (PDGFRβ+CD146+Nes+). While both types are able to proliferate in response to glycerol or BaCl₂-induced injury, type-1 pericytes give rise to adipogenic cells only in response to glycerol injection and type-2 become myogenic in response to both types of injury. The extent to which type-1 pericytes participate in fat accumulation is not known.

Pericytes are also associated with endothelial cell differentiation and multiplication, angiogenesis, survival of apoptotic signals and travel. Certain pericytes, known as microvascular pericytes, develop around the walls of capillaries and help to serve this function. Microvascular pericytes may not be contractile cells, as they lack alpha-actin isoforms, structures that are common amongst other contractile cells. These cells communicate with endothelial cells via gap junctions, and in turn cause endothelial cells to proliferate or be selectively inhibited. If this process did not occur, hyperplasia and abnormal vascular morphogenesis could result. These types of pericyte can also phagocytose exogenous proteins. This suggests that the cell type might have been derived from microglia.

A lineage relationship to other cell types has been proposed, including smooth muscle cells, neural cells, NG2 glia, muscle fibers, adipocytes, as well as fibroblasts and other mesenchymal stem cells. However, whether these cells differentiate into each other is an outstanding question in the field. Pericytes' regenerative capacity is affected by aging. Such versatility is useful, as they actively remodel blood vessels throughout the body and can thereby blend homogeneously with the local tissue environment.

Aside from creating and remodeling blood vessels, pericytes have been found to protect endothelial cells from death via apoptosis or cytotoxic elements. It has been shown in vivo that pericytes release a hormone known as pericytic aminopeptidase N/pAPN that may help to promote angiogenesis. When this hormone was mixed with cerebral endothelial cells as well as astrocytes, the pericytes grouped into structures that resembled capillaries. Furthermore, when the experimental group contained all of the following with the exception of pericytes, the endothelial cells would undergo apoptosis. ^{[further explanation needed]} It was thus concluded that pericytes must be present to ensure the proper function of endothelial cells, and astrocytes must be present to ensure that both remain in contact. If not, then proper angiogenesis cannot occur. It has also been found that pericytes contribute to the survival of endothelial cells, as they secrete the protein Bcl-w during cellular crosstalk. Bcl-w is an instrumental protein in the pathway that enforces VEGF-A expression and discourages apoptosis. Although there is some speculation as to why VEGF is directly responsible for preventing apoptosis, it is believed to be responsible for modulating apoptotic signal transduction pathways and inhibiting activation of apoptosis-inducing enzymes. Two biochemical mechanisms utilized by VEGF to accomplish this would be phosphorylation of extracellular regulatory kinase 1 (ERK-1, also known as MAPK3), which sustains cell survival over time, and inhibition of stress-activated protein kinase/c-jun-NH2 kinase, which also promotes apoptosis.