Open AccessNanoparticle targeting of de novo profibrotic macrophages mitigates lung fibrosis
Author(s) -
Abhalaxmi Singh,
Sreeparna Chakraborty,
Sing Wan Wong,
Nicole A Hefner,
Andrew Stuart,
Abdul S Qadir,
Asok Mukhopadhyay,
Kurt Bachmaier,
JaeWon Shin,
Jalees Rehman,
Asrar B. Malik
Publication year - 2022
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.2121098119
Subject(s) - fibrosis , pulmonary fibrosis , macrophage , extracellular matrix , mannose receptor , cancer research , monocyte , scavenger receptor , immunology , biology , microbiology and biotechnology , medicine , pathology , endocrinology , lipoprotein , biochemistry , cholesterol , in vitro
Significance Current therapies for pulmonary fibrosis (PF) focus on slowing disease progression and reducing functional decline in patients by dampening the activation of fibroblasts and other implicated cells. There is a need for strategies that target the essential cells and signaling pathways involved in disease pathogenesis. Monocyte-derived macrophages (Mo-Macs) are known to express profibrotic genes and are involved in the pathogenesis of PF. Our results show that engineered mannosylated albumin nanoparticles specifically targeted disease-inducing Mo-Macs, and further, that nanoparticles efficiently delivered small-interfering RNA against profibrotic cytokine tumor growth factor β1 to prevent bleomycin-induced lung fibrosis.