• 2007.sition pore, allowing the Mn to pass freely thus presumably caus-ing the mitochondrial alterations seen in this study [36]. (fliphtml5.com)
  • These involve the activation of Jak/STAT3 and PI3K/Akt, which subsequently decreases mitochondrial permeability transition pore (mPTP) opening and increases mitochondrial K ATP (Mito K ATP ) channel opening, which attenuates myocardial ischaemia reperfusion injury. (researchgate.net)
  • A major effect of the polar fraction was to promote cyclosporin A (CsA)-sensitive permeability transition pore (PTP) opening in isolated liver mitochondria. (nih.gov)
  • Disruption of this balance leads to mitochondrial fragmentation, loss of mitochondrial DNA (mtDNA) integrity, and cell death [ 3 , 7 ]. (krcp-ksn.org)
  • generation, decrease of membrane potential (ΔΨm), loss of mitochondrial membrane mass, and induction of apoptosis. (nih.gov)
  • Mitochondrial dysfunction plays a critical role in the progression of acute kidney injury and chronic kidney disease. (krcp-ksn.org)
  • This review provides a comprehensive overview of the role of mitochondrial dysfunction in acute kidney injury and chronic kidney disease. (krcp-ksn.org)
  • We discuss the processes that control mitochondrial stress responses to kidney injury and review recent advances in understanding the role of mitochondrial dysfunction in inflammation and tissue damage through the use of different experimental models of kidney disease. (krcp-ksn.org)
  • Mitochondrial dysfunction arising from disturbances in the regulation of the mitochondrial electron transport chain (ETC), proton gradient, and membrane potential results in reduced adenosine triphosphate (ATP) and increased production of mitochondrial-derived reactive oxygen species (mROS), which promotes kidney injury and inflammation [ 3 , 4 ]. (krcp-ksn.org)
  • Although the cause of the metabolic deterioration is unknown, several hypotheses have been proposed, including mitochondrial dysfunction, oxidative stress, endoplasmic reticulum (ER) stress, hyperglycemia (glucotoxicity), dyslipidemia (lipotoxicity), and the combination of both (glucolipotoxicity). (e-dmj.org)
  • Parkinson's disease (PD) is the second most common neurodegenerative disease worldwide, and accumulating evidence indicates that mitochondrial dysfunction is associated with progressive deterioration in PD patients. (biomolther.org)
  • Mitochondrial dysfunction is considered a key pathogenic event of PD and contributes to the degeneration of dopaminergic neurons by activating inflammation and oxidative stress. (biomolther.org)
  • We show that reoxygenation after prolonged hypoxia reduces the reactive oxygen species (ROS) threshold for the mitochondrial permeability transition (MPT) in cardiomyocytes and that cell survival is steeply negatively correlated with the fraction of depolarized mitochondria. (nih.gov)
  • MPP + /MPTP selectively inhibits complex I in the mitochondrial electron transport chain, which consequently leads to oxidative stress and impaired calcium homeostasis. (biomolther.org)
  • MPTP treatment increased the abundance of mitochondrial fission proteins such as dynamin-related protein 1 (Drp1) and phospho-Drp1 Ser616. (biomolther.org)
  • Our findings demonstrated that sinapic acid protects against MPTP-induced PD and these effects might be related to the inhibiting abnormal mitochondrial fission through REV-ERB α. (biomolther.org)
  • Various studies have shown that MPTP changes mitochondrial quality control mechanisms, including fission and fusion. (biomolther.org)
  • Once phosphorylated/ activated, tyrosine-phosphorylated STAT3 shuttles into the nucleus and initiates stress-responsive gene transcription, 96 97 serine-phosphorylated STAT3 moves to mitochondria to regulate the mitochondrial respiratory chain 97 98 (Fig. 3). (researchgate.net)
  • Mitochondrial fusion maintains functional mitochondria and prevents the generation of defective mtDNA [ 8 ]. (krcp-ksn.org)
  • Mitochondrial responses to specific stimuli are highly regulated and synergistically modulated by tightly interconnected processes, including mitochondrial dynamics (fission, fusion) and mitophagy. (krcp-ksn.org)
  • A decrease in mitochondrial fusion promotes fission-induced mitochondrial fragmentation, but a reduction in mitochondrial fission produces excessive mitochondrial elongation. (krcp-ksn.org)
  • The equilibrium between mitochondrial fusion and fission maintains healthy mitochondrial structure and function [ 6 ]. (krcp-ksn.org)
  • Thus, modulation of mitochondrial fission and fusion might be a promising therapeutic candidate for PD. (biomolther.org)
  • Fusion is mediated through fusion proteins in the outer and inner mitochondrial membranes (OMM and IMM) called mitofusins (MFN1, MFN2) and optic atrophy 1 (OPA1), respectively [ 9 ]. (krcp-ksn.org)
  • The GTPase activity of MFN1 is higher than that of MFN2, and OPA1 fails to execute the process of mitochondrial fusion in the absence of MFN1 [ 9 , 10 ]. (krcp-ksn.org)
  • Mitochondrial swelling and fragmentation and impaired mitochondrial metabolism are directly linked to the deterioration of kidney function [ 5 ]. (krcp-ksn.org)
  • Although the aliphatic fraction failed to perturb mitochondrial function, the aromatic fraction increased the Ca 2+ retention capacity at low doses and induced mitochondrial swelling and a decrease in ΔΨm at high doses. (nih.gov)
  • Defective mitochondrial function disrupts cellular redox potential and can cause cell death. (krcp-ksn.org)
  • Sinapic acid also improved mitochondrial function in the PD models. (biomolther.org)
  • Cell protection that exhibits a memory (preconditioning) results from triggered mitochondrial swelling that causes enhanced substrate oxidation and ROS production, leading to redox activation of PKC, which inhibits glycogen synthase kinase-3beta (GSK-3beta). (nih.gov)
  • Alternatively, receptor tyrosine kinase or certain G protein-coupled receptor activation elicits cell protection (without mitochondrial swelling or durable memory) by inhibiting GSK-3beta, via protein kinase B/Akt and mTOR/p70(s6k) pathways, PKC pathways, or protein kinase A pathways. (nih.gov)
  • Endothelial swelling, perivascular edema, and mononuclear cell infiltration are the primary histologic findings. (medscape.com)
  • This swelling effect was mostly CsA insensitive and could be reproduced by a mixture of PAHs present in DEPs. (nih.gov)
  • CONCLUSION: Hence, it can be concluded that albumin nanoparticles constitute a viable method for delivering MTX and CUR to inflamed joints simultaneously, because of the strong affinity of albumin and enhanced permeability and retention effect at the inflamed joint. (bvsalud.org)