PMID- 37524487
OWN - NLM
STAT- MEDLINE
DCOM- 20230802
LR  - 20230905
IS  - 1557-8925 (Electronic)
IS  - 1054-3589 (Linking)
VI  - 98
DP  - 2023
TI  - Anti-fibrotic strategies and pulmonary fibrosis.
PG  - 179-224
LID - S1054-3589(23)00019-4 [pii]
LID - 10.1016/bs.apha.2023.04.002 [doi]
AB  - Idiopathic pulmonary fibrosis (IPF) results from the dysregulated process of 
      injury and repair, which promotes scarring of the lung tissue and deposition of 
      collagen-rich extracellular matrix (ECM) components, that make the lung 
      unphysiologically stiff. IPF presents a serious concern as its pathogenesis 
      remains elusive, and current anti-fibrotic treatments are only effective in 
      slowing rather than halting disease progression. The IPF disease pathogenesis is 
      incompletely defined, complex and incorporates interplay between different 
      fibrogenesis signaling pathways. Preclinical IPF experimental models used to 
      validate drug candidates present significant limitations in modeling IPF 
      pathobiology, with their limited time frame, simplicity and inaccurate 
      representation of the disease and the mechanical influences of IPF. Potentially 
      more accurate mimetic disease models that capture the cell-cell and cell-matrix 
      interaction, such as 3D cultures, organoids and precision-cut lung slices (PCLS), 
      may yield more meaningful clinical predictions for drug candidates. Recent 
      advances in developing anti-fibrotic compounds have positioned drug towards 
      targeting components of the fibrogenesis signaling pathway of IPF or the 
      extracellular microenvironment. The major goals in this area of research focus on 
      finding ways to reverse or halt the disease progression by utilizing more 
      disease-relevant experimental models to improve the qualification of potential 
      drug targets for treating pulmonary fibrosis.
CI  - Copyright (c) 2023. Published by Elsevier Inc.
FAU - Gunatilaka, Avanka
AU  - Gunatilaka A
AD  - Department of Biochemistry and Pharmacology, The University of Melbourne, 
      Parkville, VIC, Australia; ARC Centre for Personalised Therapeutics Technologies, 
      The University of Melbourne, Parkville, VIC, Australia.
FAU - Zhang, Stephanie
AU  - Zhang S
AD  - Department of Biochemistry and Pharmacology, The University of Melbourne, 
      Parkville, VIC, Australia.
FAU - Tan, Wan Shun Daniel
AU  - Tan WSD
AD  - Department of Biochemistry and Pharmacology, The University of Melbourne, 
      Parkville, VIC, Australia.
FAU - G Stewart, Alastair
AU  - G Stewart A
AD  - Department of Biochemistry and Pharmacology, The University of Melbourne, 
      Parkville, VIC, Australia; ARC Centre for Personalised Therapeutics Technologies, 
      The University of Melbourne, Parkville, VIC, Australia. Electronic address: 
      astew@unimelb.edu.au.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20230427
PL  - United States
TA  - Adv Pharmacol
JT  - Advances in pharmacology (San Diego, Calif.)
JID - 9015397
SB  - IM
MH  - Humans
MH  - Fibrosis
MH  - *Idiopathic Pulmonary Fibrosis/drug therapy/metabolism/pathology
MH  - Disease Progression
OTO - NOTNLM
OT  - Anti-fibrotic compounds
OT  - Extracellular matrix
OT  - Fibrogenesis signaling pathways
OT  - Fibrosis experimental models
OT  - Idiopathic pulmonary fibrosis
OT  - Lung fibrosis
OT  - Nintedanib
OT  - Pirfenidone
EDAT- 2023/08/01 01:08
MHDA- 2023/08/02 06:42
CRDT- 2023/07/31 20:56
PHST- 2023/08/02 06:42 [medline]
PHST- 2023/08/01 01:08 [pubmed]
PHST- 2023/07/31 20:56 [entrez]
AID - S1054-3589(23)00019-4 [pii]
AID - 10.1016/bs.apha.2023.04.002 [doi]
PST - ppublish
SO  - Adv Pharmacol. 2023;98:179-224. doi: 10.1016/bs.apha.2023.04.002. Epub 2023 Apr 
      27.