Role of mitochondrial autophagy mediated by PINK1/Parkin signaling pathway in severe pneumonia_West China Medical Journal

Authors：

SHI Rui ¹ ,  SHAO Yaxin ² , TIAN Xiaoyu ³ , CAI Lingling ⁴

1. Department of Pediatrics, Huairou Hospital, Beijing Hospital of Traditional Chinese Medicine, Beijing 101400, P. R. China;
2. Department of Pediatrics, Pinggu Hospital, Beijing Hospital of Traditional Chinese Medicine, Beijing 101299, P. R. China;
3. Department of Emergency Medicine, Huairou Hospital, Beijing Hospital of Traditional Chinese Medicine, Beijing 101400, P. R. China;
4. Department of Dermatology, Dongfang Hospital of Beijing University of Chinese Medicine (Second Clinical Medical College of Beijing University of Chinese Medicine), Beijing 100078, P. R. China;

Corresponding?author：

SHAO Yaxin, Email: cux7343@163.com

Keywords：

Severe pneumonia; mitochondrial autophagy; homologous phosphatase tensin induced kinase 1; Parkinson’s protein; signaling pathway

DOI：

10.7507/1002-0179.202308104

Video：

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Abstract Full text Figures/Tables Video References Cited by

Objective To investigate the role of mitochondrial autophagy mediated by PINK1 (homologous phosphatase tensin induced kinase 1) /Parkin (Parkinson’s protein) signaling pathway in severe pneumonia of rats. Methods Twenty rats were randomly divided into control group and model group (severe pneumonia model), with 10 rats in each group, to explore the effects of severe pneumonia on lung function and pathology in rats. Then, 30 rats were randomly divided into control group, model group and mdivi-1 (mitochondrial autophagy inhibitor) group, with 10 rats in each group, to further explore the effects of severe pneumonia on mitochondrial autophagy indicators of rats. Results Compared with the control group, the resting ventilation volume [(3.44±0.22) vs. (1.58±0.18) mL/min] and airway resistance ratio (77.48±3.84 vs. 47.76±5.54) in the model group were decreased (P<0.05). In the model group, the lung tissue was injured and a large number of inflammatory cells were infiltrated. The protein and mRNA expression levels of Parkin, PINK1 and microtubule-associated protein1 light chain 3 in lung tissues of model group were increased (P<0.05). Compared with model group, the ratio of resting ventilator-to-airway resistance in mdivi-1 group increased (P<0.05). The injury and inflammatory infiltration of lung tissue were improved in mdivi-1 group. The expression levels of Parkin, PINK1 and microtubule-associated protein1 light chain 3 protein and mRNA in lung tissues of mdivi-1 group were decreased (P<0.05). Conclusion Mdivi-1 can improve the abnormal lung function structure in rats with severe pneumonia, and the mechanism may be related to mitochondrial autophagy mediated by PINK1/Parkin signaling pathway.

Citation： SHI Rui, SHAO Yaxin, TIAN Xiaoyu, CAI Lingling. Role of mitochondrial autophagy mediated by PINK1/Parkin signaling pathway in severe pneumonia. West China Medical Journal, 2024, 39(4): 567-572. doi: 10.7507/1002-0179.202308104 Copy

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7.	陳興, 李紅衛, 趙永健, 等. Pink1/Parkin介導的線粒體自噬在急性肺損傷中的作用研究進展. 吉林醫學, 2022, 43(12): 3334-3337.
8.	劉燕, 趙星, 劉邦祺. 重慶市沙坪壩區重癥肺炎患者流行病學調查. 公共衛生與預防醫學, 2021, 32(4): 146-149.
9.	羅成, 葉遠航, 盛國光, 等. 中醫藥治療重癥肺炎的研究進展. 中國中醫急癥, 2023, 32(5): 929-932.
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11.	郭楓, 樂道平, 陳晶, 等. 烏司他丁聯合美羅培南對老年重癥肺炎患者炎癥介質和氧化應激的影響. 中國老年學雜志, 2022, 42(9): 2134-2136.
12.	胡婧, 周玉玲, 劉坤. 橙皮苷對重癥肺炎大鼠肺組織炎癥和細胞凋亡影響. 中國免疫學雜志, 2023, 39(4): 727-732, 738.
13.	Zhuang N, Li L, Chen S, et al. PINK1-dependent phosphorylation of PINK1 and Parkin is essential for mitochondrial quality control. Cell Death Dis, 2016, 7(12): e2501.
14.	Wang N, Zhu P, Huang R, et al. PINK1: the guard of mitochondria. Life Sci, 2020, 259: 118247.
15.	Miao CC, Hwang W, Chu LY, et al. LC3A-mediated autophagy regulates lung cancer cell plasticity. Autophagy, 2022, 18(4): 921-934.

1. Nair GB, Niederman MS. Updates on community acquired pneumonia management in the ICU. Pharmacol Ther, 2021, 217: 107663.
2. Klionsky DJ, Petroni G, Amaravadi RK, et al. Autophagy in major human diseases. EMBO J, 2021, 40(19): e108863.
3. 王健齡. PINK1/Parkin介導的線粒體自噬在無機砷調節肺臟巨噬細胞極化中的作用研究. 唐山: 華北理工大學, 2022.
4. Imberechts D, Kinnart I, Wauters F, et al. DJ-1 is an essential downstream mediator in PINK1/parkin-dependent mitophagy. Brain, 2022, 145(12): 4368-4384.
5. Mora AL, Bueno M, Rojas M. Mitochondria in the spotlight of aging and idiopathic pulmonary fibrosis. J Clin Invest, 2017, 127(2): 405-414.
6. Ito A, Hashimoto M, Tanihata J, et al. Involvement of Parkin-mediated mitophagy in the pathogenesis of chronic obstructive pulmonary disease-related sarcopenia. J Cachexia Sarcopenia Muscle, 2022, 13(3): 1864-1882.
7. 陳興, 李紅衛, 趙永健, 等. Pink1/Parkin介導的線粒體自噬在急性肺損傷中的作用研究進展. 吉林醫學, 2022, 43(12): 3334-3337.
8. 劉燕, 趙星, 劉邦祺. 重慶市沙坪壩區重癥肺炎患者流行病學調查. 公共衛生與預防醫學, 2021, 32(4): 146-149.
9. 羅成, 葉遠航, 盛國光, 等. 中醫藥治療重癥肺炎的研究進展. 中國中醫急癥, 2023, 32(5): 929-932.
10. 裴飛, 吳健鋒. 重癥肺炎與炎癥風暴: 共識與爭議. 中國實用內科雜志, 2022, 42(3): 182-185.
11. 郭楓, 樂道平, 陳晶, 等. 烏司他丁聯合美羅培南對老年重癥肺炎患者炎癥介質和氧化應激的影響. 中國老年學雜志, 2022, 42(9): 2134-2136.
12. 胡婧, 周玉玲, 劉坤. 橙皮苷對重癥肺炎大鼠肺組織炎癥和細胞凋亡影響. 中國免疫學雜志, 2023, 39(4): 727-732, 738.
13. Zhuang N, Li L, Chen S, et al. PINK1-dependent phosphorylation of PINK1 and Parkin is essential for mitochondrial quality control. Cell Death Dis, 2016, 7(12): e2501.
14. Wang N, Zhu P, Huang R, et al. PINK1: the guard of mitochondria. Life Sci, 2020, 259: 118247.
15. Miao CC, Hwang W, Chu LY, et al. LC3A-mediated autophagy regulates lung cancer cell plasticity. Autophagy, 2022, 18(4): 921-934.

West China Medical Journal

Role of mitochondrial autophagy mediated by PINK1/Parkin signaling pathway in severe pneumonia

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