Common Biomarkers in Chronic Obstructive Pulmonary Disease and Bronchopulmonary Dysplasia: A Narrative Review of an Intriguing Interplay

Bronchopulmonary dysplasia (BPD) is a chronic lung condition in preterm infants characterized by impaired alveolar development, disrupted vascular growth, and persistent inflammation. These alterations, which often arise from early exposure to mechanical ventilation, oxygen toxicity, and infection, can lead to long-term structural and functional deficits in the developing lung. In adulthood, chronic obstructive pulmonary disease (COPD) represents a major cause of morbidity and mortality and is defined by progressive airflow obstruction, reduced respiratory capacity, and chronic inflammatory responses. Although traditionally considered a disease of adult smokers, growing evidence suggests that early-life respiratory insults play a key role in shaping long-term lung health. Recent studies reveal a biologically plausible link between BPD and later COPD, indicating that premature birth, impaired lung growth, and early inflammatory injury may predispose individuals to earlier or more severe COPD development. This review explores the shared molecular pathways connecting these conditions, focusing on overlapping inflammatory biomarkers such as <i>IL1B</i>, <i>IL6</i>, <i>IL8</i>, <i>TNF</i>, <i>TGFB</i>, and <i>VEGF</i>, which collectively reflect persistent dysregulation of immune and repair mechanisms. Additionally, common genetic variants, including <i>SERPINA1</i> and <i>HHIP</i>, may contribute to susceptibility across the lifespan. Emerging biomarkers-such as <i>PRMT7</i>, <i>cathelicidin</i>/<i>LL-37</i>, <i>CRISPLD2</i>, and <i>GDF15</i>-offer further insight into disease progression. Identifying these shared markers may ultimately improve early detection and help clinicians pinpoint infants with BPD who face an elevated risk of developing COPD later in life.