ArticleCurrent medical science2020
Mitofusion 2 Overexpression Decreased Proliferation of Human Embryonic Lung Fibroblasts in Acute Respiratory Distress Syndrome through Inhibiting RAS-RAF-1-ERK1/2 Pathway.
Article in Current medical science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 3 citations in OpenAlex.
- Targeting of miR-93-5p/Mfn2 Axis Attenuates Lung Fibrosis in Rats With Acute Respiratory Distress Syndrome by Regulating Endoplasmic Reticulum Stress.Physiological research · 2025Article
- Mitochondrial fusion protein: a new therapeutic target for lung injury diseases.Frontiers in physiology · 2025Review
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4 authors at 1 institution in 1 country.
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Abstract
Acute respiratory distress syndrome (ARDS) is one of the most fatal diseases worldwide. Pulmonary fibrosis occurs early in ARDS, and its severity plays a crucial role in ARDS mortality rate. Some studies suggested that fibroproliferation is an essential mechanism in ARDS. Mitofusion2 (Mfn2) overexpression plays a role in inhibiting cell proliferation. However, the role and potential mechanism of Mfn2 on the proliferation of fibroblasts is still unknown. In this study, we aimed at exploring the effect of Mfn2 on the human embryonic lung fibroblasts (HELF) and discussed its related mechanism. The HELF were treated with the Mfn2 overexpressing lentivirus (adv-Mfn2). The cell cycle was detected by flow cytometry. MTT, PCR and Western blotting were used to investigate the effect of Mfn2 on the proliferation of the HELF, collagen expression, the RAS-RAF-1-ERK1/2 pathway and the expression of cycle-related proteins (p21, p27, Rb, Raf-1, p-Raf-1, Erk1/2 and p-Erk1/2). The co-immunoprecipitation assay was used to explore the interaction between Mfn2 and Ras. The results showed that the overexpression of Mfn2 inhibited the proliferation of the HELF and induced the cell cycle arrest at the G
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