Elastin peptides derived from the elastin-rich connective tissue of the fish cardiac arterial bulb (bulbus arteriosus) represent a distinctive, highly bioavailable source of extracellular matrix (ECM) repair substrates for the respiratory system.

Targeted enzymatic hydrolysis yields low-molecular weight peptides (≈500-700 Da) that are efficiently absorbed via PepT1 and retain the cross-linking amino acids desmosine and isodesmosine - the molecular “fingerprints” essential for elastin network reconstruction.

Functionally homologous to alveolar recoil and pulmonary vascular compliance, these peptides act through a triad of mechanisms:

• substrate provision for tropoelastin synthesis and cross-linking;
• signaling modulation (elastin-derived peptide/EBP-integrin pathways) that supports balanced matrix turnover; and
• protective effects that dampen elastase/MMP overactivation and oxidative stress.

Collectively, these actions target key structures - alveoli, airways, interstitium, and pulmonary vasculature - where chronic inflammation and oxidative injury degrade elastin fibers, lower tissue compliance, and drive fibrotic remodeling.

In the pulmonary interstitium, incorporation of desmosine / isodesmosine-containing fragments helps rebalance collagen-elastin composition and counter fibroblast over-activation, supporting anti-fibrotic trajectories.

In the vascular wall, these peptides reinforce elastin cross-linking (LOX/LOXL axis), improve compliance, and help preserve repair outcomes by anti-protease and antioxidant activity, complementing vasodilator / anti-proliferative pharmacotherapies.

This structural-first, protection-enabled framework provides a translational rationale for nutritional interventions aimed at restoring ECM integrity and function across COPD, IPF, pulmonary hypertension, and post-COVID-19 respiratory sequelae.