Role of elastic fiber degradation in disease pathogenesis.
Level 5 - mechanism / opinion, no new human data
Narrative review of pathophysiological mechanisms without systematic synthesis or new empirical data.
PubMed 37001705 · doi:10.1016/j.bbadis.2023.166706
What was done
This narrative review summarizes evidence on the role of elastic fiber degradation in the pathogenesis and clinical manifestations of hereditary disorders, aging, and disease across different organ systems, including the vasculature, lungs, eyes, and joints.
What was found
The abstract reports no quantitative data or effect sizes. Qualitatively, it highlights that adult tissues synthesize minimal new elastin, rendering elastic fiber damage largely permanent. Degradation disrupts biomechanical homeostasis and produces elastin degradation products that provoke inflammatory responses, serving as a shared pathological feature across diverse diseases and co-morbidities.
Why it matters
Understanding elastic fiber breakdown as a common mechanism across multiple tissues explains shared phenotypes and co-morbidities in aging and hereditary disorders. It emphasizes stabilizing elastic matrix structures and restoring elastin as key therapeutic targets.
Limits
The abstract describes a narrative overview rather than a systematic review or meta-analysis, with no defined search protocol, study selection criteria, or risk-of-bias evaluation. No quantitative human or clinical outcome metrics are reported.
Cited by
- supports Aging causes a substantial loss of the connective tissue protein elastin throughout the entire body.