Current Studies of Mitochondrial Quality Control in the Preeclampsia

Peng, Xiaoqing; Hou, Ruirui; Yang, Yuanyuan; Luo, Zhigang; Cao, Yunxia

doi:10.3389/fcvm.2022.836111

Cited by 6 publications

(4 citation statements)

References 120 publications

(166 reference statements)

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“…Mitochondria are tiny structures within cells responsible for energy production and maintaining normal cellular functions. Studies have indicated that there may be abnormalities in mitochondrial function in the cells of pre-eclampsia patients ( 41 , 42 ). This relationship can be explored in several ways: Firstly, Damage to cells from an excess of oxygen free radical generation occurs in pre-eclampsia patients due to oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Identification and verification of diagnostic biomarkers based on mitochondria-related genes related to immune microenvironment for preeclampsia using machine learning algorithms

Huang,

Song,

Yang

et al. 2024

Front. Immunol.

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Preeclampsia is one of the leading causes of maternal and fetal morbidity and mortality worldwide. Preeclampsia is linked to mitochondrial dysfunction as a contributing factor in its progression. This study aimed to develop a novel diagnostic model based on mitochondria-related genes(MRGs) for preeclampsia using machine learning and further investigate the association of the MRGs and immune infiltration landscape in preeclampsia. In this research, we analyzed GSE75010 database and screened 552 DE-MRGs between preeclampsia samples and normal samples. Enrichment assays indicated that 552 DE-MRGs were mainly related to energy metabolism pathway and several different diseases. Then, we performed LASSO and SVM-RFE and identified three critical diagnostic genes for preeclampsia, including CPOX, DEGS1 and SH3BP5. In addition, we developed a novel diagnostic model using the above three genes and its diagnostic value was confirmed in GSE44711, GSE75010 datasets and our cohorts. Importantly, the results of RT-PCR confirmed the expressions of CPOX, DEGS1 and SH3BP5 were distinctly increased in preeclampsia samples compared with normal samples. The results of the CIBERSORT algorithm revealed a striking dissimilarity between the immune cells found in preeclampsia samples and those found in normal samples. In addition, we found that the levels of SH3BP5 were closely associated with several immune cells, highlighting its potential involved in immune microenvironment of preeclampsia. Overall, this study has provided a novel diagnostic model and diagnostic genes for preeclampsia while also revealing the association between MRGs and immune infiltration. These findings offer valuable insights for further research and treatment of preeclampsia.

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Section: Discussionmentioning

confidence: 99%

Identification and verification of diagnostic biomarkers based on mitochondria-related genes related to immune microenvironment for preeclampsia using machine learning algorithms

Huang,

Song,

Yang

et al. 2024

Front. Immunol.

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“…In addition, BNIP3 serves as a mitophagy receptor in the ubiquitin-independent pathway, interacts directly with LC3 or recruits Parkin, and participates in hypoxia-mediated mitophagy (Fu et al, 2020). Mounting evidence suggests that ubiquitin-independent mitophagy may play a more crucial role in PE compared with the ubiquitin-dependent pathway (Peng et al, 2022). Zhou et al showed that BNIP3 was downregulated along with autophagic dysfunction and mitochondria injury in PE placentae (Zhou et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

6-Gingerol alleviates placental injury in preeclampsia by inhibiting oxidative stress via BNIP3/LC3 signaling-mediated trophoblast mitophagy

Li,

Zhao,

Yang

et al. 2023

Front. Pharmacol.

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Background and aims: Preeclampsia (PE) is the leading cause of maternal and fetal morbidity and mortality worldwide. Apoptosis of trophoblast cells induced by oxidative stress is a principal reason of placental injury in PE. 6-Gingerol, an antioxidant from ginger, plays an important role in many disease models, but its effect on obstetric diseases has not been elucidated. In this study, we investigated the protective effect of 6-gingerol against placental injury.Methods:In vitro hypoxia/reoxygenation (H/R) model of HTR8/Svneo cells and preeclamptic mice model were established to simulate PE. The effects of 6-Gingerol on PE were evaluated by morphological detection, biochemical analysis, and Western blot.Results: We found that H/R treatment induced cell apoptosis, increased the production of reactive oxygen species, malondialdehyde and lactate dehydrogenase, and decreased superoxide dismutase in trophoblast. In addition, the polarization of mitochondrial membrane potential and the cellular calcium flux were also destroyed under H/R condition, which also activated BCL2-interacting protein 3 (BNIP3) and provoked excessive mitophagy. Importantly, 6-Gingerol reversed these corrosive effects. Furthermore, the placenta damage in PE-like mouse caused by the cell apoptosis, oxidative stress and mitophagy was mitigated by 6-Gingerol.Conclusion: These findings suggest that 6-Gingerol exerts a protective effect against placental injury in PE by reducing oxidative stress and inhibiting excessive mitophagy caused by mitochondrial dysfunction.

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“…Peripheral fission induces the division of damaged components in mitochondria with low mitochondrial membrane potential (MMP), which are divided into smaller mitochondria and then cleaned from the mitochondrial network through mitophagy. If lacking the timely and innocuous removal of impaired mitochondrial content, substances such as Ca 2+ or cytochrome c can be released into the cytosol, leading to irrevers-ible cell death [81][82][83]. Therefore, the above two mitochondrial fission subtypes are both important aspects of MQC that function to maintain mitochondrial homeostasis.…”

Section: Mitochondrial Quality Control and Aicmentioning

confidence: 99%

The Role of Mitochondrial Quality Control in Anthracycline-Induced Cardiotoxicity: From Bench to Bedside

Lin

Peng

et al. 2022

Oxidative Medicine and Cellular Longevity

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Cardiotoxicity is the major side effect of anthracyclines (doxorubicin, daunorubicin, epirubicin, and idarubicin), though being the most commonly used chemotherapy drugs and the mainstay of therapy in solid and hematological neoplasms. Advances in the field of cardio-oncology have expanded our understanding of the molecular mechanisms underlying anthracycline-induced cardiotoxicity (AIC). AIC has a complex pathogenesis that includes a variety of aspects such as oxidative stress, autophagy, and inflammation. Emerging evidence has strongly suggested that the loss of mitochondrial quality control (MQC) plays an important role in the progression of AIC. Mitochondria are vital organelles in the cardiomyocytes that serve as the key regulators of reactive oxygen species (ROS) production, energy metabolism, cell death, and calcium buffering. However, as mitochondria are susceptible to damage, the MQC system, including mitochondrial dynamics (fusion/fission), mitophagy, mitochondrial biogenesis, and mitochondrial protein quality control, appears to be crucial in maintaining mitochondrial homeostasis. In this review, we summarize current evidence on the role of MQC in the pathogenesis of AIC and highlight the therapeutic potential of restoring the cardiomyocyte MQC system in the prevention and intervention of AIC.

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Current Studies of Mitochondrial Quality Control in the Preeclampsia

Cited by 6 publications

References 120 publications

Identification and verification of diagnostic biomarkers based on mitochondria-related genes related to immune microenvironment for preeclampsia using machine learning algorithms

Identification and verification of diagnostic biomarkers based on mitochondria-related genes related to immune microenvironment for preeclampsia using machine learning algorithms

6-Gingerol alleviates placental injury in preeclampsia by inhibiting oxidative stress via BNIP3/LC3 signaling-mediated trophoblast mitophagy

The Role of Mitochondrial Quality Control in Anthracycline-Induced Cardiotoxicity: From Bench to Bedside

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