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Condition: Mitochondrial Disease

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Total 454 results found since Jan 2013.

Melatonin attenuates doxorubicin-induced cardiotoxicity through preservation of YAP expression.
In this study, we examined the possible protective effects of melatonin on doxorubicin-induced cardiotoxicity and explored the underlying mechanisms related to this process. We found that in vitro doxorubicin treatment significantly decreased H9c2 cell viability and induced apoptosis as manifested by increased TUNEL-positive cells, down-regulation of anti-apoptotic protein Bcl-2, as well as up-regulation of pro-apoptotic protein Bax. This was associated with increased reactive oxygen species (ROS) levels and decreased mitochondrial membrane potentials (MMP). In vivo, five weeks of doxorubicin treatment significantly decrea...
Source: J Cell Mol Med - February 17, 2020 Category: Molecular Biology Authors: Li HR, Wang C, Sun P, Liu DD, Du GQ, Tian JW Tags: J Cell Mol Med Source Type: research

Elevated Aldolase 1A, retrogene 1 expression induces cardiac apoptosis in rat experimental autoimmune myocarditis model.
Abstract Acute myocarditis is an unpredictable heart disease, which is caused by inflammation-associated cell death. Although viral infection and drug exposure are known to induce acute myocarditis, the molecular basis for its development remains undefined. Using proteomics and molecular analyses in myosin-induced rat experimental autoimmune myocarditis (EAM), we identified that elevated expression of aldolase 1A, retrogene 1 (Aldoart1) is critical to induce mitochondrial dysfunction and acute myocarditis development. Here, we demonstrate that cardiac cell death is associated with increased expressions of pro-apop...
Source: Canadian Journal of Physiology and Pharmacology - January 29, 2020 Category: Drugs & Pharmacology Authors: Choi S, Chung JH, Nam MH, Bang E, Hong KS, Kim YH, Seo JB, Chi SG Tags: Can J Physiol Pharmacol Source Type: research

Embelin averts MPTP-induced dysfunction in mitochondrial bioenergetics and biogenesis via activation of SIRT1
Publication date: Available online 24 January 2020Source: Biochimica et Biophysica Acta (BBA) - BioenergeticsAuthor(s): Swetha Pavani Rao, Neelam Sharma, Shasi V. KalivendiAbstractParkinson's disease (PD) is a chronic neurodegenerative disease characterized by the death of dopamine neurons of Substantia nigra pars compacta (SNpc) leading to motor deficits. Amongst the mechanisms proposed, mitochondrial dysfunction, reduced complex-I and PGC1α levels were found to correlate with the pathology of PD. As embelin is a natural product with structural resemblance to ubiquinone, exhibits mitochondrial uncoupling and antioxidant ...
Source: Biochimica et Biophysica Acta (BBA) Bioenergetics - January 26, 2020 Category: Biochemistry Source Type: research

Alterations in α-synuclein and PINK1 expression reduce neurite length and induce mitochondrial fission and Golgi fragmentation in midbrain neurons
This study provides novel evidence that α-synuclein overexpression and PINK1 deletion converge to induce significant increases in Golgi fragmentation and mitochondrial fission in midbrain neurons, that are correlated with decreases in neurite length. This highlights the need for further studies on these converging mechanisms in dopaminergic neurodegeneration in PD.
Source: Neuroscience Letters - January 23, 2020 Category: Neuroscience Source Type: research

Thioredoxin-Interacting Protein (TXNIP) Regulates Parkin/PINK1-mediated Mitophagy in Dopaminergic Neurons Under High-glucose Conditions: Implications for Molecular Links Between Parkinson ’s Disease and Diabetes
In this study, we investigated the roles of thioredoxin-interacting protein (TXNIP) in Parkin/PINK1-mediated mitophagy in dopaminergic (DA) cells under high-glucose (HG) conditions. In streptozotocin-induced diab etic mice, TXNIP was upregulated and autophagy was inhibited in the midbrain, while the loss of DA neurons was accelerated by hyperglycemia. In cultured PC12 cells under HG, TXNIP expression was upregulated and the intracellular reactive oxygen species (ROS) levels increased, leading to cell death. Autophagic flux was further blocked and PINK1 expression was decreased under HG conditions. Parkin expression in the ...
Source: Neuroscience Bulletin - January 13, 2020 Category: Neuroscience Source Type: research

Extracellular mitochondrial DNA promote NLRP3 inflammasome activation and induce acute lung injury through TLR9 and NF- κB.
Conclusions: Extracellular mtDNA promote NLRP3 inflammasome activation, acute pulmonary inflammation and injury through TLR9, p38 MAPK and NF-κB pathways. PMID: 31903272 [PubMed]
Source: Journal of Thoracic Disease - January 8, 2020 Category: Respiratory Medicine Tags: J Thorac Dis Source Type: research

Mitochondrial carnitine palmitoyltransferase 2 is involved in Nε-(carboxymethyl)-lysine-mediated diabetic nephropathy
Publication date: Available online 12 December 2019Source: Pharmacological ResearchAuthor(s): Jangho Lee, Ju-Yong Hyon, Jin Young Min, Yang Hoon Huh, Hyo Jung Kim, Hayoung Lee, Sung Ho Yun, Chi-Won Choi, Su Jeong Ha, Joon Park, Young-Ho Chung, Hye Gwang Jeong, Sang Keun Ha, Sung Keun Jung, YoonSook Kim, Eun Hee HanAbstractDiabetic nephropathy (DN) is the most common cause of end-stage renal disease in the world. Advanced glycation end products (AGEs) are thought to be involved in the pathogenesis of DN via multifactorial mechanisms including the generation of oxidative stress and overproduction of various growth factors an...
Source: Pharmacological Research - December 13, 2019 Category: Drugs & Pharmacology Source Type: research

l-ornithine activates Ca2+ signaling to exert its protective function on human proximal tubular cells.
Abstract Oxidative stress and reactive oxygen species (ROS) generation can be influenced by G-protein coupled receptor (GPCR)-mediated regulation of intracellular Ca2+ ([Ca2+]i) signaling. ROS production are much higher in proximal tubular (PT) cells; in addition, the lack of antioxidants enhances the vulnerability to oxidative damage. Despite such predispositions, PT cells show resiliency, and therefore must possess some inherent mechanism to protect from oxidative damage. While the mechanism in unknown, we tested the effect of l-ornithine, since it is abundantly present in PT luminal fluid and can activate calci...
Source: Cellular Signalling - November 22, 2019 Category: Cytology Authors: Shin S, Gombedza FC, Bandyopadhyay BC Tags: Cell Signal Source Type: research

Inhibition of DNM1L and mitochondrial fission attenuates inflammatory response in fibroblast-like synoviocytes of rheumatoid arthritis.
Abstract Mitochondrial fission and fusion are important for mitochondrial function, and dynamin 1-like protein (DNM1L) is a key regulator of mitochondrial fission. We investigated the effect of mitochondrial fission on mitochondrial function and inflammation in fibroblast-like synoviocytes (FLSs) during rheumatoid arthritis (RA). DNM1L expression was determined in synovial tissues (STs) from RA and non-RA patients. FLSs were isolated from STs and treated with a DNM1L inhibitor (mdivi-1, mitochondrial division inhibitor 1) or transfected with DNM1L-specific siRNA. Mitochondrial morphology, DNM1L expression, cell vi...
Source: J Cell Mol Med - November 20, 2019 Category: Molecular Biology Authors: Wang X, Chen Z, Fan X, Li W, Qu J, Dong C, Wang Z, Ji Z, Li Y Tags: J Cell Mol Med Source Type: research

TBX3 deficiency accelerates apoptosis in cardiomyoblasts through regulation of P21 expression
In conclusion, we demonstrated that TBX3 deficiency accelerated apoptosis via directly regulating P21 expression in senescent cardiomyoblasts.
Source: Life Sciences - November 6, 2019 Category: Biology Source Type: research

Upregulation of OPA1 by carnosic acid is mediated through induction of IKK γ ubiquitination by parkin and protects against neurotoxicity.
In conclusion, the mechanism by which CA counteracts the toxicity of 6-OHDA is through modulation of mitochondrial dynamics and upregulation of OPA1 via activation of the parkin/IKKγ/p65 pathway. PMID: 31705926 [PubMed - as supplied by publisher]
Source: Food and Chemical Toxicology - November 5, 2019 Category: Food Science Authors: Lin CY, Chen WJ, Fu RH, Tsai CW Tags: Food Chem Toxicol Source Type: research

High Glucose Provokes Microvesicles Generation from Glomerular Podocytes via NOX4/ROS Pathway.
Abstract Microvesicles (MVs) were involved in the pathogenesis of many diseases, such as cardiovascular diseases and diabetes. Oxidative stress played a key role in the development and progression of diabetic nephropathy. Our aim of this study was to investigate whether high glucose could provoke microvesicles generation from podocytes and its potential mechanism. Mouse podocyte clone 5 (MPC-5) were stimulated by high glucose. The intracellular reactive oxygen species (ROS) of podocytes were measured by fluorescence microscopy with the probe of CM-H2DCFDA and MitoSOXTM. Antioxidants N-Acetyl-L-cysteine (NAC) and ...
Source: Bioscience Reports - October 29, 2019 Category: Biomedical Science Authors: Li M, Zhang T, Wu X, Chen Y, Sun L Tags: Biosci Rep Source Type: research

Beneficial effects of PGC-1 α in the substantia nigra of a mouse model of MPTP-induced dopaminergic neurotoxicity.
CONCLUSIONS: Our results indicated that PGC-1α rescues the effects of MPTP-induced mitochondrial dysfunction in C57BL mice. PMID: 31634150 [PubMed - as supplied by publisher]
Source: Aging - October 20, 2019 Category: Biomedical Science Authors: Wang Y, Chen C, Huang W, Huang M, Wang J, Chen X, Ye Q Tags: Aging (Albany NY) Source Type: research

Mitochondrial pyruvate carrier 2 mediates mitochondrial dysfunction and apoptosis in high glucose-treated podocytes
Publication date: Available online 10 October 2019Source: Life SciencesAuthor(s): Jun Feng, Yiqiong Ma, Zhaowei Chen, Jijia Hu, Qian Yang, Guohua DingAbstractAimsPodocytes play an important role in the development of diabetic kidney disease (DKD). Mitochondria are the source of energy for cell survival, and mitochondrial abnormalities have been shown to contribute to podocyte injury in DKD. In high glucose (HG)-treated podocytes, mitochondrial function and dynamics are abnormal, and intracellular metabolism is often disrupted. However, the molecular mechanism is still unclear. Mitochondrial pyruvate carrier 2 (MPC2) mediat...
Source: Life Sciences - October 10, 2019 Category: Biology Source Type: research

Liraglutide ameliorates non-alcoholic steatohepatitis by inhibiting NLRP3 inflammasome and pyroptosis activation via mitophagy.
Abstract Non-alcoholic steatohepatitis (NASH) is a key step in the progression of non-alcoholic fatty liver disease (NAFLD), which causes serious health problems worldwide. The nucleotide-binding oligomerization domain, leucine-rich repeat-containing receptor-containing pyrin domain 3 (NLRP3) inflammasome and pyroptosis play crucial roles in the progression of NASH. Our team has provided clinical evidence of the effects of glucagon-like peptide-1 (GLP-1) on the improvement in liver function and histological resolution of NAFLD. Preliminary work has demonstrated that GLP-1 inhibited NLRP3 inflammasome activation in...
Source: European Journal of Pharmacology - October 4, 2019 Category: Drugs & Pharmacology Authors: Yu X, Hao M, Liu Y, Ma X, Lin W, Xu Q, Zhou H, Shao N, Kuang H Tags: Eur J Pharmacol Source Type: research