Fibroblasts are cells that play a role in the body’s connective tissues. These spindle-shaped cells synthesize the extracellular matrix, which provides structural support to animal tissues. They are the most common cells found within connective tissue, forming a basic framework for various organs and structures.
Where Fibroblasts are Found
Fibroblasts are found throughout connective tissues. They are abundant in areas such as the skin, tendons, ligaments, and the framework of organs like the liver, lungs, and heart.
In the skin, dermal fibroblasts support epidermal layers and hair production. In bones and cartilage, fibroblasts contribute to the collagen components providing rigidity and flexibility. They also support blood vessels, like capillaries, as pericytes.
How Fibroblasts Maintain Body Structure
Fibroblasts maintain body structure by producing and organizing components of the extracellular matrix (ECM). This network, which surrounds cells, provides support, strength, and elasticity to tissues and organs. The ECM’s specific composition, determined by fibroblast activity, influences the unique properties for different connective tissues, from bone’s rigid structure to skin’s pliable nature.
Components synthesized by fibroblasts include collagen, elastin, and proteoglycans. Collagen, the most abundant protein in mammals, forms tough fiber bundles providing tensile strength to tissues like skin, tendons, and bone. Fibroblasts secrete tropocollagen, collagen’s precursor, which then assembles into triple-helical fibers outside the cell, forming scaffolding.
Elastin, another fibrous protein, gives tissues the ability to stretch and recoil, important in structures like blood vessels, lungs, and skin. Proteoglycans, along with glycosaminoglycans, form a hydrated, gel-like substance that fills spaces between cells and fibers. This matrix helps maintain tissue hydration, provides cushioning, and facilitates nutrient and waste product diffusion.
Fibroblasts in Wound Healing
Fibroblasts play a role in wound healing and tissue repair. When an injury occurs, fibroblasts from surrounding connective tissue are activated and migrate to the damage site, appearing within 24 to 48 hours post-injury. They then proliferate, increasing their numbers for repair.
Upon reaching the wound bed, these active fibroblasts deposit new extracellular matrix components, including collagen types I and III, fibronectin, and proteoglycans, replacing the fibrin clot. This new matrix forms granulation tissue, a temporary scaffold for blood vessel formation and epithelial cell migration, leading to restoration.
During healing, some fibroblasts transform into myofibroblasts. This differentiation is triggered by mechanical tension and growth factors like transforming growth factor-beta (TGF-β). Myofibroblasts acquire contractile properties, similar to smooth muscle cells, due to increased expression of alpha-smooth muscle actin. These contractile cells pull wound edges closer together in wound contraction, reducing wound size and promoting closure.
Fibroblasts and Disease
While fibroblasts are important for tissue maintenance and repair, their dysregulation can lead to fibrotic disorders. Fibrosis involves excessive accumulation of extracellular matrix components, particularly collagen, leading to tissue stiffening, scarring, and organ dysfunction. This activity results from persistent inflammatory stimuli or aberrant signaling, causing fibroblasts to remain activated and matrix-producing.
Organ fibrosis affects many body parts, leading to complications. In lung fibrosis, excessive collagen stiffens lung tissue, hindering gas exchange. Liver cirrhosis, caused by chronic injury, involves widespread fibrosis that replaces healthy liver cells, disrupting architecture. Cardiac fibrosis can similarly impair the heart’s pumping efficiency and electrical conduction, contributing to heart failure.
Dysregulated fibroblast activity can also lead to keloids and hypertrophic scars, abnormal skin injury responses. Fibroblasts proliferate and deposit disorganized collagen in the dermis. Keloids, unlike hypertrophic scars, grow beyond original wound boundaries, forming raised, often itchy, painful, and recurring lesions. Both illustrate how fibroblasts’ beneficial repair can become detrimental when uncontrolled, leading to disfigurement and functional limitations.