Tissue repair

Tissue repair works by running four overlapping stages after an injury — clotting, inflammation, proliferation, and remodelling — in which the body first stops the bleeding, then clears the damage, then fills the gap with new cells and matrix, and finally reorganises that matrix for strength. In most adult human tissue the result is a repair, meaning functional scar, rather than a true regeneration that restores the original architecture.

The four stages

1. Haemostasis (minutes). Platelets plug the wound and release growth factors that recruit everything that follows.
2. Inflammation (hours to days). Neutrophils and macrophages clear pathogens and dead tissue. See inflammation.
3. Proliferation (days to weeks). Fibroblasts migrate in and lay down type III collagen; new capillaries grow in through angiogenesis; epithelial cells close the surface.
4. Remodelling (weeks to years). Type III collagen is replaced by stronger, better-aligned type I collagen. Repaired tendon typically regains most, not all, of its original tensile strength.

Repair versus regeneration

Liver, gut lining, skin epidermis, and skeletal muscle regenerate well because they keep a reserve of stem or satellite cells. Tendon, ligament, cartilage, and heart muscle repair poorly, for two structural reasons: few resident progenitor cells and a thin blood supply. That is why most injury-focused research in this encyclopedia concentrates on those tissues.

What limits it

• Blood supply. Without new vessels, oxygen and nutrients never reach the repair site.
• Mechanical load. Collagen aligns along lines of stress, so controlled loading improves the final tissue and complete immobilisation degrades it.
• Age and metabolic state. Diabetes, smoking, and corticosteroids each slow the proliferative stage measurably.

Why peptides care

Repair-focused compounds catalogued here act at different points in the sequence:

• BPC-157 — reported to accelerate fibroblast outgrowth and migration from tendon in preclinical models.
• TB-500 — binds actin and is described as promoting cell migration and tissue remodelling.
• GHK-Cu — described as stimulating collagen, elastin, and glycosaminoglycan synthesis.
• IGF-1 LR3 — an analog of IGF-1, studied for satellite-cell activation and protein synthesis in muscle.
• Selank — early orthopaedic interest exists, but the evidence is preclinical and the compound is primarily an anxiolytic nootropic.

Human clinical data are thin across this group. Each article states its own evidence grade for every claim.