VPS33B and pulmonary fibrosis: Furthermore, this relationship between excessive collagen-I, VPS33B, and integrin α11 is also observed in chronic skin wounds, where, similar to lung fibrosis, there is a chronic unresolved wound-healing response; this is suggestive of a common pathological molecular pathway between the two organs, based on enhanced endocytic recycling of collagen-I protomers directed to fibrillogenesis.