(i) ECM structural fibrous proteins collagen and elastin, the basement membrane integral protein laminin 332, and the glycosaminoglycan hyaluronan are all degraded by lytic enzymes to expose cryptic molecular fragments (matrikines), which activate signals on nearby cells to influence physiology. (ii) MMP9 and/or MMP8 cleave ECM collagen to form fragments that are further processed by prolyl endopeptidase to release PGP, which ligates CXCR1 and CXCR2 chemokine receptors to mediate neutrophil chemotaxis into the area of injury and increase vascular permeability. (iii) Elastin fragmentation, primarily mediated by MMP12, generates VGVAPG peptides, which are chemoattractant for monocytes and are proposed to act through the S-Gal receptor. (iv) HA within basement membranes is cleaved by hyaluronidase isoforms during tissue injury to release low–molecular weight, tissue-active HA, which ligates CD44 and TLRs on epithelial cells and leukocytes to invoke appropriate inflammatory and wound healing responses to injury and prevent excessive tissue remodeling and fibrosis. (v) Laminin 332 γ subunit in basement membranes is cleaved by multiple MMPs with release of the γ₂ ectodomain peptide, an EGFR ligand that promotes epithelial proliferation to promote alveologenesis and tissue remodeling.