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Editorial
. 2012 Mar 1;185(5):475-6.
doi: 10.1164/rccm.201201-0047ED.

Biological insights from clinical trials and networks

Victor J Thannickal, James S Hagood
Editorial

Biological insights from clinical trials and networks

Victor J Thannickal et al. Am J Respir Crit Care Med. .
No abstract available

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Figures

Figure 1.
Figure 1.
Schematic of a potential mechanism by which statins may promote pulmonary fibrosis. In a COPDGene cohort of current/former smokers, statin use was found to be associated with a higher risk of interstitial lung abnormalities on high-resolution computed tomography, an effect seen in subjects of age greater than 65 years, but not in the 45- to 55-year age group; the significance of this finding was greater with hydrophilic (versus hydrophobic) statins. In an animal model of bleomycin-induced lung injury and fibrosis, pre-treatment of mice with statins increased fibrosis by a mechanism that may involve the activation of mitchondrial reactive oxygen species (mtROS) and NLRP3 inflammasome activation in macrophages (1).
See this image and copyright information in PMC

Comment on

  • Statins and pulmonary fibrosis: the potential role of NLRP3 inflammasome activation.
    Xu JF, Washko GR, Nakahira K, Hatabu H, Patel AS, Fernandez IE, Nishino M, Okajima Y, Yamashiro T, Ross JC, Estépar RS, Diaz AA, Li HP, Qu JM, Himes BE, Come CE, D'Aco K, Martinez FJ, Han MK, Lynch DA, Crapo JD, Morse D, Ryter SW, Silverman EK, Rosas IO, Choi AM, Hunninghake GM; COPDGene Investigators. Xu JF, et al. Am J Respir Crit Care Med. 2012 Mar 1;185(5):547-56. doi: 10.1164/rccm.201108-1574OC. Epub 2012 Jan 12. Am J Respir Crit Care Med. 2012. PMID: 22246178 Free PMC article.

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References

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