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Specialty: Research
Condition: Mitochondrial Disease

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Total 16 results found since Jan 2013.

VDR promotes nucleus pulposus cell mitophagy as a protective mechanism against oxidative stress injury
This study demonstrates that VDR activation ameliorates oxidative damage and decreases NP cell apoptosis by promoting PINK1/Parkin-dependent mitophagy, indicating that VDR may serve as a promising therapeutic target in the management of IDD.PMID:35786375 | DOI:10.1080/10715762.2022.2094791
Source: Free Radical Research - July 5, 2022 Category: Research Authors: Tao Lan Bin Yan Weizhuang Guo Zhe Shen Jianting Chen Source Type: research

Impact of mitochondrial transcription factor A expression on the outcomes of ovarian, endometrial and cervical cancers.
Authors: Hu W, Ma SL, Liu LL, Zhu YH, Zeng TT, Li Y, Guan XY Abstract Gynecologic cancers, including endometrial, ovarian, and cervical cancers, are the leading causes of cancer-related mortality in women worldwide. Mitochondrial transcription factor A (TFAM) has been demonstrated playing critical roles in the development of tumors. However, the clinical relationship of TFAM expression in gynecologic cancers requires further clarification. Our results showed gynecologic cancer cells are highly expressed TFAM in both protein and RNA levels compared to normal cells. The TCGA dataset revealed that TFAM gene expression...
Source: American Journal of Translational Research - October 13, 2020 Category: Research Tags: Am J Transl Res Source Type: research

Eclalbasaponin I causes mitophagy to repress oxidative stress-induced apoptosis via activation of p38 and ERK in SH-SY5Y cells.
In this study, pretreatment with EcI in SH-SY5Y cells significantly activated the p38-mitogenactivated protein kinase (p38), the extracellular regulated protein kinase (ERK), whereas it did not affect the c-jun NH2 terminal kinases (JNK). In accordance with the initial findings, EcI-induced neuroprotective effect was attenuated by SB203580 (SB, a p38 inhibitor) or FR180204 (FR, an ERK inhibitor), being further confirmed by specific small interfering RNA (siRNA). Inhibition of either p38 or ERK up-regulated the apoptosis induction in EcI- and H2O2-cotreated cells. Furthermore, p38 or ERK suppression enhanced intracellular a...
Source: Free Radical Research - June 14, 2019 Category: Research Tags: Free Radic Res Source Type: research

Albumin Overload and PINK1/Parkin Signaling-Related Mitophagy in Renal Tubular Epithelial Cells.
CONCLUSIONS In conclusion, our study suggests that mitochondrial dysfunction activates the PINK1/Parkin signaling and mitophagy in renal tubular epithelial cells under albumin overload condition. PMID: 29494565 [PubMed - in process]
Source: Medical Science Monitor - March 2, 2018 Category: Research Tags: Med Sci Monit Source Type: research

Nitro-oleic acid ameliorates oxygen and glucose deprivation/re-oxygenation triggered oxidative stress in renal tubular cells via activation of Nrf2 and suppression of NADPH oxidase.
Authors: Nie H, Xue X, Liu G, Guan G, Liu H, Sun L, Zhao L, Wang X, Chen Z Abstract Nitroalkene derivative of oleic acid (OA-NO2), due to its ability to mediate revisable Michael addition, has been demonstrated to have various biological properties and become a therapeutic agent in various diseases. Though its antioxidant properties have been reported in different models of acute kidney injury, the mechanism by which OA-NO2 attenuates intracellular oxidative stress is not well investigated. Here, we elucidated the anti-oxidative mechanism of OA -NO2 in an in vitro model of renal ischemia/reperfusion injury. Human t...
Source: Free Radical Research - August 23, 2016 Category: Research Tags: Free Radic Res Source Type: research

Acquired Mitochondrial Abnormalities, Including Epigenetic Inhibition of Superoxide Dismutase 2, in Pulmonary Hypertension and Cancer: Therapeutic Implications.
In conclusion, cancer and PAH share acquired mitochondrial abnormalities that increase proliferation and inhibit apoptosis, suggesting new therapeutic targets. PMID: 27343087 [PubMed - in process]
Source: Advances in Experimental Medicine and Biology - June 29, 2016 Category: Research Tags: Adv Exp Med Biol Source Type: research

Id: 140: klotho, an anti-aging molecule, regulates alveolar epithelial cell mtdna damage and apoptosis
Conclusions Our data demonstrate a crucial role for AEC AKT signaling in mediating the mtDNA damage protective effects of Klotho. Given the importance of AEC aging and apoptosis in pulmonary fibrosis, we reason that Klotho/AKT axis is an innovative therapeutic target for preventing common lung diseases of aging (i.e. IPF, COPD, lung cancer, etc.) for which more effective management regimens are clearly needed. Funding NIH-RO1 ES020357-01A1 (DK) and VA Merit (DK).
Source: Journal of Investigative Medicine - March 21, 2016 Category: Research Authors: Kim, S., Cheresh, P., Jablonski, R., Kamp, D., Eren, M., Vaughan, D. Tags: Pulmonary/Critical Care Source Type: research

Attenuated SAG expression exacerbates 4-hydroxy-2-nonenal-induced apoptosis and hypertrophy of H9c2 cardiomyocytes.
Authors: Park JH, Lee JH, Park JW Abstract Oxidative stress, associated with the accumulation of reactive oxygen species (ROS), results in numerous and detrimental effects on the myocardium such as the induction of apoptotic cell death, hypertrophy, fibrosis, dysfunction, and dilatation. The product of sensitive to apoptosis gene (SAG) is a RING finger protein that has been shown to have a protective effect against apoptosis induced by oxidative stress in various cell types. The major reactive aldehydic product of lipid peroxidation, 4-hydroxy-2-nonenal (HNE), is believed to be largely responsible for cytopathologi...
Source: Free Radical Research - February 18, 2016 Category: Research Tags: Free Radic Res Source Type: research

Melatonin protects hepatocytes against bile acid-induced mitochondrial oxidative stress via the AMPK-SIRT3-SOD2 pathway.
This study investigates the protective effects of melatonin pretreatment on glycochenodeoxycholic acid (GCDCA)-induced hepatotoxicity and elucidates the potential mechanism of melatonin-mediated protection. Melatonin markedly decreased mitochondrial ROS (mROS) production in L02 cells treated with 100 μM GCDCA, and inhibited GCDCA-stimulated cytotoxicity. Notably, melatonin exerted its hepatoprotective effects by upregulating sirtuin 3 (SIRT3) activity and its expression level, thus regulating superoxide dismutase 2 (SOD2) acetylation and inhibiting the production of mROS induced by GCDCA. Moreover, siRNA targeting SIRT3 b...
Source: Free Radical Research - February 18, 2016 Category: Research Tags: Free Radic Res Source Type: research

High-content genome-wide RNAi screens identify regulators of parkin upstream of mitophagy
Nature advance online publication 24 November 2013. doi:10.1038/nature12748 Authors: Samuel A. Hasson, Lesley A. Kane, Koji Yamano, Chiu-Hui Huang, Danielle A. Sliter, Eugen Buehler, Chunxin Wang, Sabrina M. Heman-Ackah, Tara Hessa, Rajarshi Guha, Scott E. Martin & Richard J. Youle An increasing body of evidence points to mitochondrial dysfunction as a contributor to the molecular pathogenesis of neurodegenerative diseases such as Parkinson’s disease. Recent studies of the Parkinson’s disease associated genes PINK1 (ref. 2) and parkin (PARK2, ref. 3) indicate that they may act in a quality control pathway ...
Source: Nature AOP - November 24, 2013 Category: Research Authors: Samuel A. HassonLesley A. KaneKoji YamanoChiu-Hui HuangDanielle A. SliterEugen BuehlerChunxin WangSabrina M. Heman-AckahTara HessaRajarshi GuhaScott E. MartinRichard J. Youle Tags: Letter Source Type: research