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Book ; Online: Mitochondria in Health and Diseases

Javadov, Sabzali / Kozlov, Andrey V. / Camara, Amadou K.S.

2020

Keywords	Medicine ; hypoglycemia ; sodium dichloroacetate ; pyruvate dehydrogenase kinase ; pyruvate dehydrogenase ; oxidative stress ; neuron death ; cholangiocellular carcinoma ; mitochondria ; energy metabolism ; oxidative phosphorylation ; 4-HNE ; DRP1 ; ERK1/2 ; hippocampus ; JNK ; mitochondrial dynamics ; PKA ; protein phosphatases ; TUNEL ; DDE ; high-fat diet ; mitochondrial UCP2 ; ROS ; antioxidant system ; uncoupling protein ; mitochondria: energy metabolism ; lipid handling ; fatty acid oxidation ; potassium channel ; reactive oxygen species ; antioxidants ; life span ; aging ; BKCa channels ; pravastatin ; gemfibrozil ; liver ; colon ; mitochondrial function ; cyclosporin A ; mitochondria calcium buffering ; mitochondria bioenergetics ; mitochondria permeability transition pore ; inorganic phosphate ; hepatic fibrogenesis ; HtrA2/Omi ; reactive oxygen species stress ; mitochondrial homeostasis ; complex I (CI) deficiency ; metabolome and proteome profiling ; reactive oxygen species (ROS) ; respirasome assembly ; electron tunneling (ET) ; perilipin 5 ; lipid droplet ; H9c2 cardiomyoblasts ; adenine nucleotide translocase ; respiratory supercomplexes ; ETC complexes ; dentate granule cell ; epilepsy ; hyperforin ; LONP1 ; neuroprotection ; pilocarpine ; seizure ; siRNA ; cardioprotection ; mitochondrial permeability transition pores ; mitochondrial connexin 43 ; cardiolipin ; iron overload ; hepcidin ; transferrin ; ferritin ; ZIP ; inflammation ; mtDNA ; mitochondrial dysfunction ; muscle aging ; physical performance ; LHON ; Siberian population ; ancient mutation ; specific genetic background ; apoptosis ; human amniotic membrane ; mitochondrial cell death ; BAX ; BCL-2 ; tensile strength ; mitochondrial gene expression ; mtDNA transcription ; mtRNA ; post-transcriptional mtRNA processing ; dsRNA ; innate immunity ; interferon response ; amino acid neurotransmitter ; cerebellar amino acid metabolism ; hypoxia ; 2-oxoglutarate dehydrogenase ; tricarboxylic acid cycle ; heart ; cytoskeletal proteins ; mitochondrial interactions ; plectin ; tubulin beta ; signaling ; GW9662 ; ischemia reperfusion injury ; Langendorff ; myocardial ; pioglitazone ; redox state ; rosiglitazone ; TZD ; uncoupling ; ADP/ATP carrier ; KmADP ; dextran ; morphology ; cardiomyocytes ; telomere length ; telomerase activity ; development ; regeneration ; intranuclear mitochondria ; healthy cells ; electron and confocal microscopy ; signaling pathways ; ion homeostasis ; human diseases
Size	1 electronic resource (434 pages)
Publisher	MDPI - Multidisciplinary Digital Publishing Institute
Publishing place	Basel, Switzerland
Document type	Book ; Online
Note	English ; Open Access
HBZ-ID	HT021044297
ISBN	9783039363858 ; 3039363859
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Book ; Online: Mitochondria: Hubs of Cellular Signaling, Energetics and Redox Balance

Camara, Amadou K. S. / Aon, Miguel A.

2017

Abstract: Poised at the convergence of most catabolic and anabolic pathways, mitochondria are the center of heterotrophic aerobic life, representing a hub in the overall metabolic network of cells. The energetic functions performed by mitochondria face the ... ...

Abstract	Poised at the convergence of most catabolic and anabolic pathways, mitochondria are the center of heterotrophic aerobic life, representing a hub in the overall metabolic network of cells. The energetic functions performed by mitochondria face the unavoidable redox hurdle of handling huge amounts of oxygen while keeping its own as well as the cellular redox environment under control. Reactive oxygen species (ROS) are produced in the respiratory chain as a result of the energy supplying function of mitochondria. Originally considered an unavoidable by-product of oxidative phosphorylation, ROS have become crucial signaling molecules when their levels are kept within physiological range. This occurs when their production and scavenging are balanced within mitochondria and cells.- Mitochondria-generated hydrogen peroxide can act as a signaling molecule within mitochondria or in the cytoplasm, affecting multiple networks that control, for example, cell cycle, stress response, cell migration and adhesion, energy metabolism, redox balance, cell contraction, and ion channels. However, under pathophysiological conditions, excessive ROS levels can happen due to either overproduction, overwhelming of antioxidant defenses, or both. Under oxidative stress, detrimental effects of ROS include oxidation of protein, lipids, and nucleic acids; mitochondrial depolarization and calcium overload; and cell-wide oscillations mediated by ROS-induced ROS release mechanisms. Mitochondrial dysfunction is central in the pathogenesis of numerous human maladies including cardiomyopathies and neurodegeneration. Diseases characterized by altered nutrient metabolism, such as diabetes and cancer, exhibit elevated ROS levels.- These may contribute to pathogenesis by increasing DNA mutation, affecting regulatory signaling and transcription, and promoting inflammation. Under metabolic stress, several ionic channels present in the inner and outer mitochondrial membranes can have pro-life and -death effects. In the present E-book, based on the Frontiers Research Topic entitled: Mitochondria: Hubs of cellular signaling, energetics and redox balance, we address one of the fundamental questions that the field of ROS biology faces today: how do mitochondria accomplish a reliable energy provision and at the same time keep ROS levels within physiological, non-harming, limits but crucial for cellular signaling function? Additionally, and within the perspective of mitochondria as signaling-energetic hubs in the extensive cellular metabolic network, we ask how can their collective dynamics scale from the subcellular to the cellular, tissue and organ levels to affect function in health and disease
Keywords	Physiology ; Science (General)
Size	1 electronic resource (228 p.)
Publisher	Frontiers Media SA
Document type	Book ; Online
Note	English ; Open Access
HBZ-ID	HT020095943
ISBN	9782889452392 ; 2889452395
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Cardiomyocyte Adaptation to Exercise: K+ Channels, Contractility and Ischemic Injury.

Fitts, Robert H / Wang, Xinrui / Kwok, Wai-Meng / Camara, Amadou K S

International journal of sports medicine

2024

Abstract: ... This review highlights recent findings and focuses on cardiac factors with emphasis on K ...

Abstract	Cardiovascular disease is a leading cause of morbidity and mortality, and exercise-training (TRN) is known to reduce risk factors and protect the heart from ischemia and reperfusion injury. Though the cardioprotective effects of exercise are well-documented, underlying mechanisms are not well understood. This review highlights recent findings and focuses on cardiac factors with emphasis on K
Language	English
Publishing date	2024-04-22
Publishing country	Germany
Document type	Journal Article
ZDB-ID	603122-5
ISSN	1439-3964 ; 0172-4622 ; 0943-917X
ISSN (online)	1439-3964
ISSN	0172-4622 ; 0943-917X
DOI	10.1055/a-2296-7604
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Mitochondrial Calcium Handling in Isolated Mitochondria from a Guinea Pig Heart.

Mishra, Jyotsna / Camara, Amadou K S

Methods in molecular biology (Clifton, N.J.)

2022 Volume 2497, Page(s) 97–106

Abstract: Mitochondrial calcium ( ... ...

Abstract	Mitochondrial calcium (Ca
MeSH term(s)	Animals ; Calcium ; Guinea Pigs ; Heart ; Mitochondria, Heart ; Mitochondrial Membrane Transport Proteins ; Mitochondrial Permeability Transition Pore
Chemical Substances	Mitochondrial Membrane Transport Proteins ; Mitochondrial Permeability Transition Pore ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-06-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2309-1_6
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Editorial: Mitochondrial Exchangers and Transporters in Cell Survival and Death.

Kwok, Wai-Meng / Tajkhorshid, Emad / Camara, Amadou K S

Frontiers in physiology

2021 Volume 12, Page(s) 745353

Language	English
Publishing date	2021-09-08
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2021.745353
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Article: [No title information]

Fitts, Robert H. / Wang, Xinrui / Kwok, Wai-Meng / Camara, Amadou K. S.

International Journal of Sports Medicine

2024

Abstract: ... highlights recent findings and focuses on cardiac factors with emphasis on K channel ... IK) and increased content and activation of the sarcolemma K ATP channel ... of the sarcolemma K ATP channel and the increased phosphorylated glycogen synthase kinase-3β ...

Abstract	Cardiovascular disease is a leading cause of morbidity and mortality, and exercise-training (TRN) is known to reduce risk factors and protect the heart from ischemia and reperfusion injury. Though the cardioprotective effects of exercise are well-documented, underlying mechanisms are not well understood. This review highlights recent findings and focuses on cardiac factors with emphasis on K channel control of the action potential duration (APD), β-adrenergic and adenosine regulation of cardiomyocyte function, and mitochondrial Ca 2+ regulation. TRN-induced prolongation and shortening of the APD at low and high activation rates, respectively, is discussed in the context of a reduced response of the sarcolemma delayed rectifier potassium channel (IK) and increased content and activation of the sarcolemma K ATP channel. A proposed mechanism underlying the latter is presented, including the phosphatidylinositol-3kinase/protein kinase B pathway. TRN induced increases in cardiomyocyte contractility and the response to adrenergic agonists are discussed. The TRN-induced protection from reperfusion injury is highlighted by the increased content and activation of the sarcolemma K ATP channel and the increased phosphorylated glycogen synthase kinase-3β, which aid in preventing mitochondrial Ca 2+ overload and mitochondria-triggered apoptosis. Finally, a brief section is presented on the increased incidences of atrial fibrillation associated with age and in life-long exercisers.
Keywords	exercise training ; contractility ; sarcolemma K ; channels ; ischemic reperfusion
Language	English
Publishing date	2024-04-22
Publisher	Georg Thieme Verlag KG
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	603122-5
ISSN	1439-3964 ; 0172-4622 ; 0943-917X
ISSN (online)	1439-3964
ISSN	0172-4622 ; 0943-917X
DOI	10.1055/a-2296-7604
Database	Thieme publisher's database

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Article ; Online: 3D Optical Cryo-Imaging Method: A Novel Approach to Quantify Renal Mitochondrial Bioenergetics Dysfunction.

Mehrvar, Shima / Camara, Amadou K S / Ranji, Mahsa

Methods in molecular biology (Clifton, N.J.)

2021 Volume 2276, Page(s) 259–270

Abstract: Mitochondrial dysfunction contributes to various injuries and diseases. A mechanistic understanding of how dysfunctional mitochondria modulates metabolism is of paramount importance. Three-dimensional (3D) optical cryo-imager is a custom-designed device ... ...

Abstract	Mitochondrial dysfunction contributes to various injuries and diseases. A mechanistic understanding of how dysfunctional mitochondria modulates metabolism is of paramount importance. Three-dimensional (3D) optical cryo-imager is a custom-designed device that can quantify the volumetric bioenergetics of organs in small animal models. The instrument captures the autofluorescence of bioenergetics indices (NADH and FAD) from tissues at cryogenic temperature. The quantified redox ratio (NADH/FAD) is used as an optical indicator of mitochondrial redox state.
MeSH term(s)	Animals ; Cryopreservation ; Energy Metabolism ; Flavin-Adenine Dinucleotide/analysis ; Flavin-Adenine Dinucleotide/metabolism ; Frozen Sections ; Imaging, Three-Dimensional/methods ; Kidney/chemistry ; Kidney/metabolism ; Kidney/pathology ; Mitochondria/chemistry ; Mitochondria/metabolism ; Mitochondria/pathology ; NAD/analysis ; NAD/metabolism ; Optical Imaging/methods ; Oxidation-Reduction
Chemical Substances	NAD (0U46U6E8UK) ; Flavin-Adenine Dinucleotide (146-14-5)
Language	English
Publishing date	2021-05-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1266-8_20
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: LETM1: A Single Entity With Diverse Impact on Mitochondrial Metabolism and Cellular Signaling.

Natarajan, Gayathri K / Mishra, Jyotsna / Camara, Amadou K S / Kwok, Wai-Meng

Frontiers in physiology

2021 Volume 12, Page(s) 637852

Abstract: Nearly 2 decades since its discovery as one of the genes responsible for the Wolf-Hirschhorn Syndrome (WHS), the primary function of the leucine-zipper EF-hand containing transmembrane 1 (LETM1) protein in the inner mitochondrial membrane (IMM) or the ... ...

Abstract	Nearly 2 decades since its discovery as one of the genes responsible for the Wolf-Hirschhorn Syndrome (WHS), the primary function of the leucine-zipper EF-hand containing transmembrane 1 (LETM1) protein in the inner mitochondrial membrane (IMM) or the mechanism by which it regulates mitochondrial Ca
Language	English
Publishing date	2021-03-18
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2021.637852
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Article ; Online: Mitochondria in Health and Diseases.

Javadov, Sabzali / Kozlov, Andrey V / Camara, Amadou K S

Cells

2020 Volume 9, Issue 5

Abstract: Mitochondria are subcellular organelles evolved by endosymbiosis of bacteria with eukaryotic cells characteristics. They are the main source of ATP in the cell and play a pivotal role in cell life and cell death. Mitochondria are engaged in the ... ...

Abstract	Mitochondria are subcellular organelles evolved by endosymbiosis of bacteria with eukaryotic cells characteristics. They are the main source of ATP in the cell and play a pivotal role in cell life and cell death. Mitochondria are engaged in the pathogenesis of human diseases and aging directly or indirectly through a broad range of signaling pathways. However, despite an increased interest in mitochondria over the past decades, the mechanisms of mitochondria-mediated cell/organ dysfunction in response to pathological stimuli remain unknown. The Special Issue, "Mitochondria in Health and Diseases," organized by
MeSH term(s)	Animals ; Disease ; Health ; Humans ; Mitochondria/metabolism ; Models, Biological ; Molecular Targeted Therapy
Language	English
Publishing date	2020-05-09
Publishing country	Switzerland
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9051177
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Article ; Online: Time and charge/pH-dependent activation of K+ channel-mediated K+ influx and K+/H+ exchange in guinea pig heart isolated mitochondria; role in bioenergetic stability.

Malas, Kareem M / Lambert, David S / Heisner, James S / Camara, Amadou K S / Stowe, David F

Biochimica et biophysica acta. Bioenergetics

2022 Volume 1863, Issue 8, Page(s) 148908

Abstract: ... Chemiosmosis requires ion exchangers to remove Na⁺, K⁺, Ca²⁺, PO₄K⁺, the most abundant ... The effects of K⁺ uptake through ligand-specific mK⁺ channels stimulated/inhibited ...

Abstract	Mitochondria play an important role not only in producing energy for the cell but also for regulating mitochondrial and cell function depending on the cell's needs and environment. Uptake of cations, anions, and substrates requires a stable, polarized transmembrane charge potential (ΔΨ<sub>m</sub>). Chemiosmosis requires ion exchangers to remove Na<sup>+</sup>, K<sup>+</sup>, Ca<sup>2+</sup>, PO<sub>4</sub><sup>3-</sup>, and other charged species that enter mitochondria. Knowledge of the kinetics of mitochondrial (m) cation channels and exchangers is important in understanding their roles in regulating mitochondrial chemiosmosis and bioenergetics. The influx/efflux of K<sup>+</sup>, the most abundant mitochondrial cation, alters mitochondrial volume and shape by bringing in anions and H<sub>2</sub>O by osmosis. The effects of K<sup>+</sup> uptake through ligand-specific mK<sup>+</sup> channels stimulated/inhibited by agonists/antagonists on mitochondrial volume (swelling/contraction) are well known. However, a more important role for K<sup>+</sup> influx is likely its effects on H<sup>+</sup> cycling and bioenergetics facilitated by mitochondrial (m) K<sup>+</sup>/H<sup>+</sup> exchange (mKHE), though the kinetics and consequences of K<sup>+</sup> efflux by KHE are not well described. We hypothesized that a major role of K<sup>+</sup> influx/efflux is stimulation of respiration via the influx of H<sup>+</sup> by KHE. We proposed to modulate KHE activity by energizing guinea pig heart isolated mitochondria and by altering the mK<sup>+</sup> cycle to capture changes in mitochondrial volume, pH<sub>m</sub>, ΔΨ<sub>m</sub>, and respiration that would reflect a role for H<sup>+</sup> influx via KHE to regulate bioenergetics. To test this, mitochondria were suspended in a 150 mM K<sup>+</sup> buffer at pH 6.9, or in a 140 mM Cs<sup>+</sup> buffer at pH 7.6 or 6.9 with added 10 mM K<sup>+</sup>, minimal Ca<sup>2+</sup> and free of Na<sup>+</sup>. O<sub>2</sub> content was measured by a Clark electrode, and pH<sub>m</sub>, ΔΨ<sub>m</sub>, and volume, were measured by fluorescence spectrophotometry and light-scattering. Adding pyruvic acid (PA) alone caused increases in volume and respiration and a rapid decrease in the transmembrane pH gradient (ΔpH<sub>m</sub> = pH<sub>in</sub>-pH<sub>ext</sub>) at pH<sub>ext</sub> 6.9> > 7.6, so that ΔΨ<sub>m</sub> was charged and maintained. BK<sub>Ca</sub> agonist NS1619 and antagonist paxilline modified these effects, and KHE inhibitor quinine and K<sup>+</sup> ionophore valinomycin depolarized ΔΨ<sub>m</sub>. We postulate that K<sup>+</sup> efflux-induced H<sup>+</sup> influx via KHE causes an inward H<sup>+</sup> leak that stimulates respiration, but at buffer pH 6.9 also utilizes the energy of ΔpH<sub>m</sub>, the smaller component of the overall proton motive force, ΔμH<sup>+</sup>. Thus ΔpH<sub>m</sub> establishes and maintains the ΔΨ<sub>m</sub> required for utilization of substrates, entry of all cations, and for oxidative phosphorylation. Thus, K<sup>+</sup> influx/efflux appears to play a pivotal role in regulating energetics while maintaining mitochondrial ionic balance and volume homeostasis.
MeSH term(s)	Animals ; Anions/metabolism ; Energy Metabolism ; Guinea Pigs ; Hydrogen-Ion Concentration ; Ionophores/metabolism ; Ionophores/pharmacology ; Ligands ; Mitochondria, Heart/metabolism ; Potassium/metabolism ; Pyruvic Acid/metabolism ; Pyruvic Acid/pharmacology ; Quinine/metabolism ; Quinine/pharmacology ; Valinomycin/metabolism ; Valinomycin/pharmacology
Chemical Substances	Anions ; Ionophores ; Ligands ; Valinomycin (2001-95-8) ; Pyruvic Acid (8558G7RUTR) ; Quinine (A7V27PHC7A) ; Potassium (RWP5GA015D)
Language	English
Publishing date	2022-08-09
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	60-7
ISSN	1879-2650 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2650 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbabio.2022.148908
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