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How a fibroblast ages: a role for bone morphogenetic protein 4 in protecting lung fibroblasts from senescence in pulmonary fibrosis
Senin, 02 Jan 2023 11:07:32

Laszlo Farkas, Jeffrey C. Horowitz, Ana L. Mora

European Respiratory Journal 2022 60: 2201702; DOI: 10.1183/13993003.01702-2022


Idiopathic pulmonary fibrosis (IPF) is a deadly lung parenchymal disease that causes progressive scarring, functional deterioration and death [1]. Current treatments are inadequate, since they are incapable of reversing the progression of disease. Transforming growth factor-β (TGF-β) has emerged as a significant cause of fibrosis due to its stimulation of fibroblast differentiation and activation, as well as related pro-fibrotic characteristics such as apoptosis resistance, metabolic reprogramming and senescence [2]. Despite its critical importance, targeting of TGF-β has proven difficult due to its broad biological roles in immune regulation and tumour suppression, as well as tissue and vascular development and maintenance, as demonstrated in SMAD3 knockout mice [3].

This editorial summarises the findings of an article showing a role for bone morphogenetic protein 4 in protecting fibroblasts from senescence and pulmonary fibrosis and puts them into the context of the current literature


  • Conflict of interest: L. Farkas received a grant from the NIH (HL139881). J.C. Horowitz received grants from the NIH (HL141195, AG075931) and has stocks from Merck and Pfizer. A.L. Mora received grants from the NIH (HL145550, AG075931).

  • Support statement: This work was supported by the National Heart, Lung, and Blood Institute (grants HL139881 and HL145550) and the National Institute on Aging (grant AG075931). Funding information for this article has been deposited with the Crossref Funder Registry.

  • Received August 31, 2022.
  • Accepted September 29, 2022.