Abnormalities of hydrogen sulfide and glutathione pathways in mitochondrial dysfunction

Quinzii, Catarina M.; López, Luís C.

doi:10.1016/j.jare.2020.04.002

Cited by 17 publications

(5 citation statements)

References 62 publications

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“…It is tempting to speculate that environmental factors, such as the nutritional status, the metabolic state of each organ and other stresses, could affect the development of the disease, its severity, and its outcome in every patient. On the other hand, malfunctioning of the various processes in which CoQ is involved, like pyrimidine biosynthesis or H2S detoxification, probably differs depending on the specific tissue or system [27,128]. It seems that epigenetic factors are also important for the development of the disease and even for recovery after CoQ10 treatment [233].…”

Section: Discussionmentioning

confidence: 99%

“…Besides, CoQ is involved in the metabolism of some aminoacids as the electron acceptor of proline dehydrogenase 1 (PROD1) [20], and probably proline dehydrogenase 2 (PROD2) [21]. Notably, by receiving electrons from the sulfide:quinone oxidoreductase (SQOR) it participates in thedetoxification of sulfides which aresignalling molecules critical for some cellular processes, but toxic when in excess [22][23][24][25][26][27]. Reduced CoQ (CoQH2) generated by all these processes transfers its electrons to complex III in the mETC.…”

Section: Coq Biological Functionsmentioning

confidence: 99%

“…CoQ is involved such as de novo pyrimidine biosynthesis [128], or sulfide metabolism [24,26,27] further contributing to the pathology. Mitophagy has been found to be increased in primary deficiency disease models and has been proposed as a protective mechanism for CoQ biosynthesis-defective cells [129], that could have variable consequences for the pathogenesis of the disease.…”

Section: It Has Been Demonstrated That Reduction In Coq Biosynthesis ...mentioning

confidence: 99%

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Primary Coenzyme Q deficiencies: A literature review and online platform of clinical features to uncover genotype-phenotype correlations

Alcázar-Fabra

Rodríguez‐Sánchez

Trevisson

et al. 2021

Free Radical Biology and Medicine

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Section: Discussionmentioning

confidence: 99%

Section: Coq Biological Functionsmentioning

confidence: 99%

Section: It Has Been Demonstrated That Reduction In Coq Biosynthesis ...mentioning

confidence: 99%

See 1 more Smart Citation

Primary Coenzyme Q deficiencies: A literature review and online platform of clinical features to uncover genotype-phenotype correlations

Alcázar-Fabra

Rodríguez‐Sánchez

Trevisson

et al. 2021

Free Radical Biology and Medicine

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“…Scale bar: (a) ROS/MitoTracker: 100 μm; JC-1 red/JC-1 green/merge: 50 μm. Oxidative Medicine and Cellular Longevity transcription factor NF-κB and increases the generation of inflammatory factors such as IL-6, IFN7, and TNF-α; ROS can activate NF-κB, which is a significant transcription factor in the complete progress of HIF-1 activation, leading to chronic inflammation of the ovary [49,[70][71][72][73][74]. The relationship between NF-κB and HIF-1 is of major importance for inflammatory diseases.…”

Section: Discussionmentioning

confidence: 99%

Chitosan Oligosaccharides Alleviate H2O2-stimulated Granulosa Cell Damage via HIF-1α Signaling Pathway

Yang

Hong

Zheng

et al. 2022

Oxidative Medicine and Cellular Longevity

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Oocyte maturation disorder and decreased quality are the main causes of infertility in women, and granulosa cells (GCs) provide the only microenvironment for oocyte maturation through autocrine and paracrine signaling by steroid hormones and growth factors. However, chronic inflammation and oxidative stress caused by ovarian hypoxia are the largest contributors to ovarian aging and GC dysfunction. Therefore, the amelioration of chronic inflammation and oxidative stress is expected to be a pivotal method to improve GC function and oocyte quality. In this study, we detected the protective effect of chitosan oligosaccharides (COS), on hydrogen peroxide- (H2O2-) stimulated oxidative damage in a human ovarian granulosa cell line (KGN). COS significantly increased cell viability, mitochondrial function, and the cellular glutathione (GSH) content and reduced apoptosis, reactive oxygen species (ROS) content, and the levels of 8-hydroxy-2 ′ -deoxyguanosine (8-OHdG), 4-hydroxynonenal (4-HNE), hypoxia-inducible factor-1α (HIF-1α), and vascular endothelial-derived growth factor (VEGF) in H2O2-stimulated KGN cells. COS treatment significantly increased levels of the TGF-β1 and IL-10 proteins and decreased levels of the IL-6 protein. Compared with H2O2-stimulated KGN cells, COS significantly increased the levels of E2 and P4 and decreased SA-β-gal protein expression. Furthermore, COS caused significant inactivation of the HIF-1α-VEGF pathway in H2O2-stimulated KGN cells. Moreover, inhibition of this pathway enhanced the inhibitory effects of COS on H2O2-stimulated oxidative injury and apoptosis in GCs. Thus, COS protected GCs from H2O2-stimulated oxidative damage and apoptosis by inactivating the HIF-1α-VEGF signaling pathway. In the future, COS might represent a therapeutic approach for ameliorating disrupted follicle development.

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“…The mitochondria in mammalian cells work as dynamic biophysical systems and play crucial roles in the regulation of energy metabolism to control cell death and survival 21 . The JC-1 assay is widely used in apoptosis studies to re ect mitochondrial function.…”

Section: Effects Of Cst On Mitochondrial Dysfunction and Oxidative St...mentioning

confidence: 99%

Cortistatin prevents glucocorticoid-associated osteonecrosis of the femoral head via the GHSR1a/Akt pathway

Yuan

You

et al. 2022

Preprint

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Long-term use of glucocorticoids (GCs) is known to be a predominant cause of osteonecrosis of the femoral head (ONFH). Moreover, GCs can mediate apoptosis of various cell types by exaggerating oxidative stress. Previous studies have reported that the AKT pathway might be closely associated with apoptosis and metabolism of osteoblasts in ONFH mediated by GCs. We have previously found that cortistatin (CST) antagonizes oxidative stress and improves cell metabolism as well as apoptosis in several conditions. In this study, we detected that local and systemic CST expression levels were diminished in patients with ONFH compared with femoral neck fracture (FNF). In addition, a GC-induced rat ONFH model was established, which impaired bone quality and angiogenesis and improved osteoblastogenesis in the femoral head. Then, administration of CST attenuated these ONFH phenotypes in this model. Furthermore, osteoblast and endothelial cell lines were cultured and stimulated with dexamethasone (Dex) in the presence or absence of recombinant CST. As a result, Dex induced apoptosis and impaired anabolic metabolism of osteoblasts and suppressed tube formation as well as migration in endothelial cells, while additional treatment with CST reversed this damage to the cells. Moreover, blocking GHSR1a, a well-accepted receptor of CST, or blocking the AKT signaling pathway largely abolished the protective function of CST in Dex-induced disorder of the cells. Taken together, our results indicate that CST has the capability to prevent GC-induced apoptosis and metabolic disorder of osteoblasts in the pathogenesis of ONFH via the GHSR1a/AKT signaling pathway.

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Abnormalities of hydrogen sulfide and glutathione pathways in mitochondrial dysfunction

Abstract: Graphical abstract

Cited by 17 publications

References 62 publications

Primary Coenzyme Q deficiencies: A literature review and online platform of clinical features to uncover genotype-phenotype correlations

Primary Coenzyme Q deficiencies: A literature review and online platform of clinical features to uncover genotype-phenotype correlations

Chitosan Oligosaccharides Alleviate H2O2-stimulated Granulosa Cell Damage via HIF-1α Signaling Pathway

Cortistatin prevents glucocorticoid-associated osteonecrosis of the femoral head via the GHSR1a/Akt pathway

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