Idiopathic Pulmonary Fibrosis (IPF) is an epithelial-driven interstitial lung disease of unknown etiology characterized by the excessive proliferation of fibroblast populations that synthesize large amounts of extracellular matrix. In this devastating disorder, all aging hallmarks appear prematurely or are altered. This review highlights key findings about IPF characteristics recently recognized as hallmarks of aging, including mechanical alterations, inflammaging, dysbiosis, alternative splicing, and disabled macroautophagy. It also revisits the classic hallmarks of aging, which encompass stem cell exhaustion, cellular senescence, and altered intercellular communication. Enhancing our understanding of the fundamental processes that underlie the altered hallmarks of aging in IPF may facilitate the development of innovative experimental strategies to improve therapeutic outcomes.

Neutrophil extracellular traps (NETs) dysregulation is implicated in various diseases, highlighting the need for accurate quantification methods. These methods must account for the unique nature of NETs, where nuclear DNA and intracellular proteins translocate to the extracellular space. This study addresses technical approaches in the Western blot quantification of NETs-associated proteins (NAPs). Neutrophils were isolated from healthy donors, stimulated with phorbol-myristate acetate (PMA), and the expression of cathelicidin antimicrobial protein LL-37 (LL-37/hCAP18), glyceraldehyde 3-phosphate dehydrogenase (GAPDH), and β-actin was analyzed over time. LL-37/hCAP18 exhibited temporal and fraction-specific distribution patterns, while the evaluation of GAPDH and β-actin as loading controls emphasized the need for more precise tailoring when studying NETs. This work aims to improve understanding of the techniques used to measure them to make more accurate comparisons in the area of NETs research. Western blot emerges as a robust and accessible tool, shedding light on the dynamics of NAPs.