Mitochondrial transplantation attenuates lipopolysaccharide-induced acute respiratory distress syndrome

Lee, Seo-Eun; Kim, In-Hyeon; Kang, Young Cheol; Kim, Yujin; Yu, Shin-Hye; Yeo, Jeong Seon; Kwon, Iksun; Lim, Jun Hyeok; Kim, Je-Hein; Han, Kyuboem; Kim, Sung-Hwan; Kim, Chun-Hyung

doi:10.1186/s12890-024-03304-2

BMC Pulm Med

2024

DOI: 10.1186/s12890-024-03304-2

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Mitochondrial transplantation attenuates lipopolysaccharide-induced acute respiratory distress syndrome

Seo-Eun Lee,

In-Hyeon Kim,

Young Cheol Kang

et al.

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Cited by 1 publication

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Mitochondrial Transplantation Ameliorates Pulmonary Fibrosis by Suppressing Myofibroblast Activation

Lee,

Yu,

Kim

et al. 2024

IJMS

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Idiopathic pulmonary fibrosis (IPF) is a pulmonary disease characterized by excessive extracellular matrix protein deposition in the lung interstitium, subsequently causing respiratory failure. IPF still has a high medical unmet requirement due to the lack of effective treatments to inhibit disease progression. The etiology of IPF remains unclear, but mitochondrial dysfunction is considered to be associated with IPF development. Therefore, targeting mitochondrial abnormalities would be a promising strategy for treating IPF. Recently, exogenous mitochondrial transplantation has been beneficial for treating mitochondrial dysfunction. The current study aimed to examine the therapeutic effect of mitochondrial transplantation on IPF in vitro and in vivo. Mitochondria were isolated from human umbilical cord mesenchymal stem cells, referred to as PN-101. Human lung fibroblasts and human bronchial epithelial cells were exposed to transforming growth factor-β, followed by PN-101 treatment to determine the in vitro efficacy of mitochondrial transplantation. An IPF mouse model established by a single intratracheal instillation of bleomycin was utilized to determine the in vivo efficacy of the intravenously treated mitochondria. PN-101 attenuated mitochondrial damage, inhibited EMC production, and suppressed epithelial-to-mesenchymal transition in vitro. Additionally, intravenous PN-101 administration alleviated bleomycin-induced fibrotic processes in the IPF mouse model with a therapeutic context. Our data indicate that PN-101 is a novel and potential therapeutic agent for IPF.

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Mitochondrial Transplantation Ameliorates Pulmonary Fibrosis by Suppressing Myofibroblast Activation

Lee,

Yu,

Kim

et al. 2024

IJMS

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Mitochondrial transplantation attenuates lipopolysaccharide-induced acute respiratory distress syndrome

Cited by 1 publication

References 39 publications

Mitochondrial Transplantation Ameliorates Pulmonary Fibrosis by Suppressing Myofibroblast Activation

Mitochondrial Transplantation Ameliorates Pulmonary Fibrosis by Suppressing Myofibroblast Activation

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