Results 91 to 100 of about 240,768 (310)

Glimepiride, a novel sulfonylurea, does not abolish myocardial protection afforded by either ischemic preconditioning or diazoxide [PDF]

, 2001
Background: The sulfonylurea glibenclamide (Glib) abolishes the cardioprotective effect of ischemic preconditioning (IP), presumably by inhibiting mitochondrial KATP channel opening in myocytes. Glimepiride (Glim) is a new sulfonylurea reported to affect
Baxter, G.F., Lawrence, C.L., Maddock, H.L., Mocanu, M.M., Standen, N.B., Yellon, D.M.   +5 more
core  

OPA1 mutation and late-onset cardiomyopathy: mitochondrial dysfunction and mtDNA instability. [PDF]

, 2012
BackgroundMitochondrial fusion protein mutations are a cause of inherited neuropathies such as Charcot-Marie-Tooth disease and dominant optic atrophy.
Bers, Donald M, Chen, Le, Chiamvimonvat, Nipavan, Cortopassi, Gino, Davies, Vanessa, Knowlton, Anne A, Liu, Tingting, Lu, Xiyuan, Tomilov, Alexey A, Tran, Alice, Votruba, Marcela   +10 more
core   +2 more sources

HIF1α-dependent mitophagy facilitates cardiomyoblast differentiation [PDF]

, 2020
Mitophagy is thought to play a key role in eliminating damaged mitochondria, with diseases such as cancer and neurodegeneration exhibiting defects in this process.
Allen, George F. G., Ganley, Ian G., Rodger, Catherine E., Weidlich, Simone, Zhao, Jin-Feng   +4 more
core   +3 more sources

Doxorubicin‐Loaded Metal–Organic Framework for Ferroptosis‐Enhanced Chemotherapy Through Sustained Zn Release and Glutathione Peroxidase Downregulation

Advanced Healthcare Materials, EarlyView.
A robust zinc‐based metal–organic framework (ZnMOF) enables dual functions of doxorubicin delivery and sustained Zn2+ release to trigger ferroptosis‐enhnaced chemotherapy. DOX@ZnMOF effectively depletes intracellular glutathione, suppresses GPX4, and elevates reactive oxygen species, leading to efficient oxidative DNA damage and apoptosis.
Xin Ma, Chenghua Deng, Chaoyu Wang, Langston Tilman, Jinhong Li, Wenbin Lin   +5 more
wiley   +1 more source

Reversible Blockade of Complex I or Inhibition of PKCβ Reduces Activation and Mitochondria Translocation of p66\u3csup\u3eShc\u3c/sup\u3e to Preserve Cardiac Function after Ischemia [PDF]

, 2014
Aim Excess mitochondrial reactive oxygen species (mROS) play a vital role in cardiac ischemia reperfusion (IR) injury. P66Shc, a splice variant of the ShcA adaptor protein family, enhances mROS production by oxidizing reduced cytochrome c to yield H2O2 ...
Camara, Amadou K.S., Heisner, James S., Stowe, David F., Udoh, Kenechukwu B., Yang, Meiying   +4 more
core   +1 more source

Bioenergetics Consequences of Mitochondrial Transplantation in Cardiomyocytes. [PDF]

, 2020
Background Mitochondrial transplantation has been recently explored for treatment of very ill cardiac patients. However, little is known about the intracellular consequences of mitochondrial transplantation.
Ali Pour, Paria, Kenney, M Cristina, Kheradvar, Arash   +2 more
core  

Patient‐Derived 3D Bioprinted Cardiac Organoid Constructs Reveal Key Pathological Features of Duchenne Muscular Dystrophy

Advanced Healthcare Materials, EarlyView.
Patient‐derived cardiac organoids reveal key features of Duchenne muscular dystrophy cardiomyopathy, including apoptosis, oxidative stress, calcium handling defects, and mechanical remodeling. By integrating organoids into alginate–gelatin bioprinted constructs, disease phenotypes are organized into scalable 3D cardiac tissues displaying extracellular ...
Vittoria Marini, Margalida Campaner Socias, Andreas Dimopoulos, Lorenza Rinvenuto, Enrico Pozzo, Diana Stalkopf, Angelo Serafini, Sara Morri, Ashley Wang, Rita La Rovere, Yoke Chin Chai, Sveva Bollini, Geert Bultynck, H. Llewelyn Roderick, Ioannis Papantoniou, Maurilio Sampaolesi   +15 more
wiley   +1 more source

Loss of cardiac tetralinoleoyl cardiolipin in human and experimental heart failure

Journal of Lipid Research, 2007
The mitochondrial phospholipid cardiolipin is required for optimal mitochondrial respiration. In this study, cardiolipin molecular species and cytochrome oxidase (COx) activity were studied in interfibrillar (IF) and subsarcolemmal (SSL) cardiac ...
Genevieve C. Sparagna, Adam J. Chicco, Robert C. Murphy, Michael R. Bristow, Christopher A. Johnson, Meredith L. Rees, Melissa L. Maxey, Sylvia A. McCune, Russell L. Moore   +8 more
doaj   +1 more source

Enhanced Na\u3csup\u3e+\u3c/sup\u3e/H\u3csup\u3e+\u3c/sup\u3e Exchange During Ischemia and Reperfusion Impairs Mitochondrial Bioenergetics and Myocardial Function [PDF]

, 2008
Inhibition of Na+/H+ exchange (NHE) during ischemia reduces cardiac injury due to reduced reverse mode Na+/Ca2+ exchange. We hypothesized that activating NHE-1 at buffer pH 8 during ischemia increases mitochondrial oxidation, Ca2+ overload, and reactive ...
Aldakkak, Mohammed, Camara, Amadou K.S., Heisner, James S., Spence, Marisha, Stowe, David F.   +4 more
core   +1 more source

Cardiac myocyte-specific knock-out of calcium-independent phospholipase A2γ (iPLA2γ) decreases oxidized fatty acids during ischemia/reperfusion and reduces infarct size [PDF]

, 2016
Calcium-independent phospholipase A(2)γ (iPLA(2)γ) is a mitochondrial enzyme that produces lipid second messengers that facilitate opening of the mitochondrial permeability transition pore (mPTP) and contribute to the production of oxidized fatty acids ...
Abendschein, Dana, Gibson Dilthey, Beverly, Gross, Richard W, Guan, Shaoping, Jenkins, Christopher M, Kovacs, Attila, Liu, Xinping, Mancuso, David J, Moon, Sung Ho, Nguyen, Annie L, Sims, Harold F, Weinheimer, Carla J, Yang, Kui   +12 more
core   +2 more sources