keyword
MENU ▼
Read by QxMD icon Read
search

mitochondrial damage

keyword
https://www.readbyqxmd.com/read/29353219/blocking-mitochondrial-cyclophilin-d-ameliorates-tsh-impaired-defensive-barrier-of-artery
#1
Xiaojing Liu, Heng Du, Qiang Chai, Qing Jia, Lu Liu, Meng Zhao, Jun Li, Hui Tang, Wenbin Chen, Lifang Zhao, Li Fang, Ling Gao, Jiajun Zhao
AIMS: Endothelial cells (ECs) constitute the defensive barrier of vasculature, which maintains the vascular homeostasis. Mitochondrial oxidative stress (mitoOS) in ECs significantly affects the initiation and progression of vascular diseases. The higher serum thyroid stimulating hormone (TSH) level is being recognized as a nonconventional risk factor responsible for the increased risk of cardiovascular diseases in subclinical hypothyroidism (SCH). However, effects and underlying mechanisms of elevated TSH on ECs are still ambiguous...
January 9, 2018: Redox Biology
https://www.readbyqxmd.com/read/29352520/ipragliflozin-improves-mitochondrial-abnormalities-in-renal-tubules-induced-by-a-high-fat-diet
#2
Susumu Takagi, Jinpeng Li, Yuta Takagaki, Munehiro Kitada, Kyoko Nitta, Toshiyuki Takasu, Keizo Kanasaki, Daisuke Koya
OBJECTIVE: Complete mechanisms of reno-protective effects of SGLT2 inhibitors have not been elucidated yet. Mitochondrial biogenesis is regulated by membrane GTPases, such as Opa1 and Mfn2. Here, we investigated whether SGLT2 inhibition in mice fed with a high-fat diet (HFD) improved mitochondrial morphology and restored mitochondrial biogenesis-related molecules. MATERIALS AND METHODS: Mice were fed in control diet or HFD with or without ipragliflozin treatment...
January 20, 2018: Journal of Diabetes Investigation
https://www.readbyqxmd.com/read/29352505/p53-independent-noxa-induction-by-cisplatin-is-regulated-by-atf3-atf4-in-head-and-neck-squamous-cell-carcinoma-cells
#3
Kanika Sharma, Thien-Trang Vu, Wade Cook, Mitra Naseri, Kevin Zhan, Wataru Nakajima, Hisashi Harada
The platinum-based DNA damaging agent cisplatin is used as a standard therapy for locally advanced head and neck squamous cell carcinoma (HNSCC). However, the mechanisms underpinning the cytotoxic effects of this compound are not entirely elucidated. Cisplatin produces anticancer effects primarily via activation of the DNA damage response, followed by inducing BCL-2 family-dependent mitochondrial apoptosis. We have previously demonstrated that cisplatin induces the expression of pro-apoptotic BCL-2 family protein, Noxa, that can bind to the pro-survival BCL-2 family protein, MCL-1, to inactivate its function and induce cell death...
January 19, 2018: Molecular Oncology
https://www.readbyqxmd.com/read/29352139/mitochondrial-glutamine-metabolism-via-got2-supports-pancreatic-cancer-growth-through-senescence-inhibition
#4
Seungyeon Yang, Sunsook Hwang, Minjoong Kim, Sung Bin Seo, Jeong-Hwa Lee, Seung Min Jeong
Cellular senescence, which leads to a cell cycle arrest of damaged or dysfunctional cells, is an important mechanism to restrain the malignant progression of cancer cells. Because metabolic changes underlie many cell-fate decisions, it has been suggested that cell metabolism might play key roles in senescence pathways. Here, we show that mitochondrial glutamine metabolism regulates senescence in human pancreatic ductal adenocarcinoma (PDAC) cells. Glutamine deprivation or inhibition of mitochondrial aspartate transaminase (GOT2) results in a profound induction of senescence and a suppression of PDAC growth...
January 19, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29351884/crucial-role-of-chelatable-iron-in-silver-nanoparticles-induced-dna-damage-and-cytotoxicity
#5
Agnieszka Grzelak, Maria Wojewódzka, Sylwia Meczynska-Wielgosz, Mariusz Zuberek, Dominika Wojciechowska, Marcin Kruszewski
Damage to mitochondria and subsequent ROS leakage is a commonly accepted mechanism of nanoparticle toxicity. However, malfunction of mitochondria results in generation of superoxide anion radical (O2•-), which due to the relatively low chemical reactivity is rather unlikely to cause harmful effects triggered by nanoparticles. We show that treatment of HepG2 cells with silver nanoparticles (AgNPs) resulted in generation of H2O2 instead of O2•-, as measured by ROS specific mitochondrial probes. Moreover, addition of a selective iron chelator diminished AgNPs toxicity...
January 9, 2018: Redox Biology
https://www.readbyqxmd.com/read/29351587/heat-exposure-induces-oxidative-stress-and-dna-damage-in-the-male-germ-line
#6
Brendan J Houston, Brett Nixon, Jacinta H Martin, Geoffry N D E Iuliis, Elizabeth G Bromfield, Kristen E McEwen, R John Aitkena
The reproductive consequences of global warming are not currently understood. In order to address this issue we have examined the reproductive consequences of exposing male mice to a mild heat stress. For this purpose, adult male mice were exposed to an elevated ambient temperature of 35°C under two exposure models. The first involved acute exposure for 24 hours, followed by recovery periods of between 1 day and 6 weeks. The alternative heating regimen involved a daily exposure of 8 hours for periods of 1 or 2 weeks...
January 17, 2018: Biology of Reproduction
https://www.readbyqxmd.com/read/29351515/understanding-key-mechanisms-of-exercise-induced-cardiac-protection-to-mitigate-disease-current-knowledge-and-emerging-concepts
#7
Bianca C Bernardo, Jenny Y Y Ooi, Kate L Weeks, Natalie L Patterson, Julie R McMullen
The benefits of exercise on the heart are well recognized, and clinical studies have demonstrated that exercise is an intervention that can improve cardiac function in heart failure patients. This has led to significant research into understanding the key mechanisms responsible for exercise-induced cardiac protection. Here, we summarize molecular mechanisms that regulate exercise-induced cardiac myocyte growth and proliferation. We discuss in detail the effects of exercise on other cardiac cells, organelles, and systems that have received less or little attention and require further investigation...
January 1, 2018: Physiological Reviews
https://www.readbyqxmd.com/read/29351463/intermediary-metabolism-and-fatty-acid-oxidation-novel-targets-of-electron-transport-chain-driven-injury-during-ischemia-and-reperfusion
#8
Qun Chen, Masood S Younus, Jeremy Thompson, Ying Hu, John M Hollander, Edward J Lesnefsky
BACKGROUND: Cardiac ischemia-reperfusion (IR) damages the electron transport chain (ETC) causing mitochondrial and cardiomyocyte injury. Reversible blockade of the ETC at complex I during ischemia protects the ETC and decreases cardiac injury. In the present study, we used an unbiased proteomic approach to analyze the extent of ETC-driven mitochondrial injury during IR. METHODS: Isolated-perfused mouse (C57BL/6) hearts underwent 25 min global ischemia (37{degree sign}C) and 30 min reperfusion...
December 29, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29351413/mitochondrial-content-is-preserved-throughout-disease-progression-in-the-mdx-mouse-model-of-duchenne-muscular-dystrophy-regardless-of-taurine-supplementation
#9
Robert G Barker, Victoria L Wyckelsma, Hongyang Xu, Robyn M Murphy
Mitochondrial dysfunction is a pathological feature of Duchenne muscular Dystrophy (DMD), a debilitating and fatal neuromuscular disorder characterised by progressive muscle wasting and weakness. Mitochondria are a source of cellular ATP and involved in Ca2+ regulation and apoptotic signalling. Ameliorating aberrant mitochondrial function has therapeutic potential for reducing DMD disease severity. The dystrophic mdx mouse exhibits peak muscle damage at 21-28d which stabilises after 8 weeks. The amino acid taurine is implicated in mitochondrial health and function, with endogenous concentrations low when measured during the cycle of peak muscle damage in mdx mice...
December 20, 2017: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/29351246/addition-of-berberine-to-preservation-solution-in-an-animal-model-of-ex-vivo-liver-transplant-preserves-mitochondrial-function-and-bioenergetics-from-the-damage-induced-by-ischemia-reperfusion
#10
Rui Miguel Martins, Anabela Pinto Rolo, João Soeiro Teodoro, Emanuel Furtado, Rui Caetano Oliveira, José Guilherme Tralhão, Carlos Marques Palmeira
Liver transplantation is a therapeutic regimen to treat patients with non-malignant end-stage liver diseases and malignant tumors of hepatic origin. The ischemia/reperfusion (I/R) injury in liver transplantation is associated with disruption of mitochondrial function in the hepatic parenchyma. Several studies have been conducted in animal models to identify pharmacological therapeutic strategies to minimize the injury induced by the cold/warm I/R in liver transplantation. Most of these studies were conducted in unrealistic conditions without the potential to be translated to clinical usage...
January 19, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29350822/resveratrol-suppresses-rotenone-induced-neurotoxicity-through-activation-of-sirt1-akt1-signaling-pathway
#11
Hui Wang, Xiaoguang Dong, Zengxun Liu, Shaowei Zhu, Haili Liu, Wenchuang Fan, Yanlai Hu, Tao Hu, Yonghui Yu, Yizhao Li, Tianwei Liu, Chengjia Xie, Qing Gao, Guibao Li, Jing Zhang, Zhaoxi Ding, Jinhao Sun
Rotenone is a common pesticide and has been reported as one of the risk factors for Parkinson disease. Rotenone can cause neuronal death or apoptosis through inducing oxidative injury and inhibiting mitochondrial function. As a natural polyphenolic compound, resveratrol possesses the anti-oxidant capacity and neuroprotective effect. However, the mechanism underlying the neuroprotective effect of resveratrol against rotenone-induced neurotoxicity remains elusive. Here, we treated PC12 cells with rotenone to induce neurotoxicity, and the neurotoxic cells were subjected to resveratrol treatment...
January 19, 2018: Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology
https://www.readbyqxmd.com/read/29348835/simultaneous-quantification-of-dna-damage-and-mitochondrial-copy-number-by-long-run-dna-damage-quantification-lord-q
#12
Benjamin Dannenmann, Simon Lehle, Sebastian Lorscheid, Stephan M Huber, Frank Essmann, Klaus Schulze-Osthoff
DNA damage and changes in the mitochondrial DNA content have been implicated in ageing and cancer development. To prevent genomic instability and tumorigenesis, cells must maintain the integrity of their nuclear and mitochondrial DNA. Advances in the research of DNA damage protection and genomic stability, however, also depend on the availability of techniques that can reliably quantify alterations of mitochondrial DNA copy numbers and DNA lesions in an accurate high-throughput manner. Unfortunately, no such method has been established yet...
December 22, 2017: Oncotarget
https://www.readbyqxmd.com/read/29348566/phosphorylation-of-ulk1-by-ampk-is-essential-for-mouse-embryonic-stem-cell-self-renewal-and-pluripotency
#13
Jiaqi Gong, Haifeng Gu, Lin Zhao, Liang Wang, Pinglei Liu, Fuping Wang, Haoyu Xu, Tongbiao Zhao
Autophagy is a catabolic process to degrade both damaged organelles and aggregated proteins in somatic cells. We have recently identified that autophagy is an executor for mitochondrial homeostasis in embryonic stem cell (ESC), and thus contribute to stemness regulation. However, the regulatory and functional mechanisms of autophagy in ESC are still largely unknown. Here we have shown that activation of ULK1 by AMPK is essential for ESC self-renewal and pluripotency. Dysfunction of Ulk1 decreases the autophagic flux in ESC, leading to compromised self-renewal and pluripotency...
January 18, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29348410/oxidative-stress-via-inhibition-of-the-mitochondrial-electron-transport-and-nrf-2-mediated-anti-oxidative-response-regulate-the-cytotoxic-activity-of-plumbagin
#14
Arvinder Kapur, Thomas Beres, Kavya Rathi, Amruta P Nayak, Austin Czarnecki, Mildred Felder, Amani Gillette, Spencer S Ericksen, Emmanuel Sampene, Melissa C Skala, Lisa Barroilhet, Manish S Patankar
Plumbagin, an anti-cancer agent, is toxic to cells of multiple species. We investigated if plumbagin targets conserved biochemical processes. Plumbagin induced DNA damage and apoptosis in cells of diverse mutational background with comparable potency. A 3-5 fold increase in intracellular oxygen radicals occurred in response to plumbagin. Neutralization of the reactive oxygen species by N-acetylcysteine blocked apoptosis, indicating a central role for oxidative stress in plumbagin-mediated cell death. Plumbagin docks in the ubiquinone binding sites (Q0 and Qi) of mitochondrial complexes I-III, the major sites for oxygen radicals...
January 18, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29348263/phosphoinositide-3-kinase-gamma-inhibition-protects-from-anthracycline-cardiotoxicity-and-reduces-tumor-growth
#15
Mingchuan Li, Valentina Sala, Maria Chiara De Santis, James Cimino, Paola Cappello, Nicola Pianca, Anna Di Bona, Jean Piero Margaria, Miriam Martini, Edoardo Lazzarini, Flora Pirozzi, Luca Rossi, Irene Franco, Julia Bornbaum, Jacqueline Heger, Susanne Rohrbach, Alessia Perino, Carlo G Tocchetti, Braulio H F Lima, Mauro M Teixeira, Paolo E Porporato, Rainer Schulz, Annalisa Angelini, Marco Sandri, Pietro Ameri, Sebastiano Sciarretta, Roberto César P Lima-Júnior, Marco Mongillo, Tania Zaglia, Fulvio Morello, Francesco Novelli, Emilio Hirsch, Alessandra Ghigo
Background -Anthracyclines, such as doxorubicin (DOX), are potent anti-cancer agents for the treatment of solid tumors and hematological malignancies. However, their clinical use is hampered by cardiotoxicity. This study sought to investigate the role of PI3Kγ in DOX-induced cardiotoxicity and the potential cardio-protective and anti-cancer effects of PI3Kγ inhibition. Methods -Mice expressing a kinase-inactive PI3Kγ or receiving PI3Kγ selective inhibitors were subjected to chronic DOX treatment. Cardiac function was analyzed by echocardiography and DOX-mediated signaling was assessed in whole hearts or in isolated cardiomyocytes...
January 18, 2018: Circulation
https://www.readbyqxmd.com/read/29348169/lipid-mediated-signals-that-regulate-mitochondrial-biology
#16
Jason R Nielson, Jared P Rutter
For decades, lipids were assumed to fulfill roles only in energy storage and membrane structure. Recent studies have discovered critical roles for phospholipids, sphingolipids, and sterols in many cellular pathways, including cell signaling and transcriptional regulation. Frequently, lipids from these various classes work together to achieve defined cellular outcomes. Specific mitochondrial lipids are critical for proper assembly of the electron transport chain complexes and for effective responses to mitochondrial damage, including maintenance of mitochondrial protein homeostasis, regulation of mitophagy, and induction of apoptosis...
January 18, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29348134/cerebral-mitochondrial-microangiopathy-leads-to-leukoencephalopathy-in-mitochondrial-neurogastrointestinal-encephalopathy
#17
L L Gramegna, A Pisano, C Testa, D N Manners, R D'Angelo, E Boschetti, F Giancola, L Pironi, L Caporali, M Capristo, M L Valentino, G Plazzi, C Casali, M T Dotti, G Cenacchi, M Hirano, C Giordano, P Parchi, R Rinaldi, R De Giorgio, R Lodi, V Carelli, C Tonon
BACKGROUND AND PURPOSE: Mitochondrial neurogastrointestinal encephalopathy is a rare disorder due to recessive mutations in the thymidine phosphorylase gene, encoding thymidine phosphorylase protein required for mitochondrial DNA replication. Clinical manifestations include gastrointestinal dysmotility and diffuse asymptomatic leukoencephalopathy. This study aimed to elucidate the mechanisms underlying brain leukoencephalopathy in patients with mitochondrial neurogastrointestinal encephalopathy by correlating multimodal neuroradiologic features to postmortem pathology...
January 18, 2018: AJNR. American Journal of Neuroradiology
https://www.readbyqxmd.com/read/29346115/mitochondrial-dysfunction-a-key-player-in-the-pathogenesis-of-cardiovascular-diseases-linked-to-air-pollution
#18
REVIEW
Sri Rahavi Boovarahan, Gino A Kurian
Air pollution has become an environmental burden with regard to non-communicable diseases, particularly heart disease. It has been reported that air pollution can accelerate the development of heart failure and atrial fibrillation. Air pollutants encompass various particulate matters (PMs), which change the blood composition and heart rate and eventually leads to cardiac failure by triggering atherosclerotic plaque ruptures or by developing irreversible ischemia. A series of major epidemiological and observational studies have established the noxious effect of air pollutants on cardiovascular diseases (CVD), but the underlying molecular mechanisms of its susceptibility and the pathological disease events remain largely elusive and are predicted to be initiated in the cell organelle...
January 18, 2018: Reviews on Environmental Health
https://www.readbyqxmd.com/read/29344415/rhizoma-coptidis-and-berberine-as-a-natural-drug-to-combat-aging-and-aging-related-diseases-via-anti-oxidation-and-ampk-activation
#19
REVIEW
Zhifang Xu, Wei Feng, Qian Shen, Nannan Yu, Kun Yu, Shenjun Wang, Zhigang Chen, Seiji Shioda, Yi Guo
Aging is the greatest risk factor for human diseases, as it results in cellular growth arrest, impaired tissue function and metabolism, ultimately impacting life span. Two different mechanisms are thought to be primary causes of aging. One is cumulative DNA damage induced by a perpetuating cycle of oxidative stress; the other is nutrient-sensing adenosine monophosphate-activated protein kinase (AMPK) and rapamycin (mTOR)/ ribosomal protein S6 (rpS6) pathways. As the main bioactive component of natural Chinese medicine rhizoma coptidis (RC), berberine has recently been reported to expand life span in Drosophila melanogaster, and attenuate premature cellular senescence...
December 2017: Aging and Disease
https://www.readbyqxmd.com/read/29343810/mitochondrial-dna-damage-and-subsequent-activation-of-z-dna-binding-protein-1-links-oxidative-stress-to-inflammation-in-epithelial-cells
#20
Bartosz Szczesny, Michela Marcatti, Akbar Ahmad, Mauro Montalbano, Attila Brunyánszki, Sofia-Iris Bibli, Andreas Papapetropoulos, Csaba Szabo
This report identifies mitochondrial DNA (mtDNA) as a target and active mediator that links low-level oxidative stress to inflammatory response in pulmonary epithelial cells. Extrusion of mtDNA into the bronchoalveolar lavage fluid occurs as an early event in mice subjected to cigarette smoke injury, concomitantly with the depletion of mtDNA in the lung tissue. In cultured lung epithelial cells, prolonged, low-level oxidative stress damages the mtDNA, without any detectable damage to the nuclear DNA. In turn, cellular depletion of the mtDNA occurs, together with a transient remodeling of cellular bioenergetics and morphology - all without any detectable impairment in overall cell viability...
January 17, 2018: Scientific Reports
keyword
keyword
65232
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"