Mitochondrial Volume Control

Garlid, Keith D.

doi:10.1007/978-1-4899-2551-0_23

Cited by 23 publications

(14 citation statements)

References 69 publications

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“…Nevertheless, cation leaks occur at signi cant rates in respiring mitochondria, and they are physiologically important. Inward potassium leak causes matrix swelling (3), and inward proton leak dissipates energy and contributes to the basal metabolic rate (4).…”

Section: Potassium Leak Across the Inner Membranementioning

confidence: 99%

The Mitochondrial Potassium Cycle

Garlid

Pauček²

2001

IUBMB Life

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SummaryThe mitochondrial K + cycle consists of in ux and ef ux pathways for K + and anions. Net movement of K + salts across the inner membrane causes changes of matrix volume, so regulation of the cycle is vital for maintaining the structural integrity of the organelle. The mitochondrial K+ cycle also appears to play important roles in cellular pathophysiology in vivo. Opening the mitochondrial ATP-sensitive K + channel (mitoK ATP ) prior to ischemia protects the heart from ischemia-reperfusion injury. MitoK ATP is an important player in the cell signaling pathways for ischemic protection and also for gene transcription, roles that appear to depend on the ability of mitoK ATP opening to trigger increased mitochondrial production of reactive oxygen species. MitoK ATP opening during both ischemia and reperfusion and during the high work state is found to preserve the structure of the intermembrane space and thereby maintains the normally low outer membrane permeability to adenine nucleotides. This review discusses the properties of the mitochondrial K + cycle that help to understand the basis of these effects.IUBMB Life, 52: 153-158, 2001

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Section: Potassium Leak Across the Inner Membranementioning

confidence: 99%

The Mitochondrial Potassium Cycle

Garlid

Pauček²

2001

IUBMB Life

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“…First advances in mK + ATP research demonstrated that different drugs stimulate the opening of mK + ATP channels decreasing mitochondrial potential (Δ m ) and that mK + ATP channels are involved in mechanisms regulating cell volume (Garlid, 1988). Latter, it was observed that bradykinin (Yang et al, 2004), opioids (Jang et al, 2008), and adenosine (Kin H, 2005), activate signaling cascades that induce the opening of mK + ATP and provide cardioprotection against ischemia/reperfusion injury.…”

Section: Mitochondrial K Atp Channelsmentioning

confidence: 99%

Oxidative Stress and Mitochondrial Dysfunction in Cardiovascular Diseases

Hernández‐Reséndiz¹,

Buelna‐Chontal²,

Correa³

et al. 2012

Oxidative Stress and Diseases

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“…The last hypothesis considers the only well-defined physiological function of mitochondrial K + transporters -the regulation of the matrix volume [163]. Stimulation of K + influx causes an increase in matrix volume [147], which has been shown to improve the rate of oxidative phosphorylation by activating fatty acid oxidation, respiration and ATP synthesis [164].…”

Section: K + Channelsmentioning

confidence: 99%

Prevention of cell damage in ischaemia: novel molecular targets in mitochondria

Morin¹,

Papadopoulos²,

Tillement³

2002

Expert Opinion on Therapeutic Targets

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Ischaemia results in a decrease of blood supply to an organ. It may be sudden or progressive, partial or complete. In any case, the lack of oxygen induces a decrease in ATP generation followed by a reduction of cellular energy-dependent processes. When ischaemia is followed by a reperfusion, the efflux of oxygen in an anoxied organ promotes an excess of reactive oxygen species (ROS) generation, which impairs the restoration of ATP synthesis. Both effects induce cellular alterations that can lead to cell death in both necrotic and apoptotic forms. As ATP synthesis and ROS generation both occur in mitochondria, they are obvious targets for pharmacological interventions aiming to prevent or block deleterious effects induced by a lack of oxygen. Different approaches may be used according to the state of the pathological process under investigation. In general, prevention of the ischaemic process is more successful than the cure of the following reperfusion state. This review summarises pharmacological strategies designed to improve cellular protection before or during ischaemia-reperfusion acting via the mitochondria and highlights promising new mitochondrial targets to be considered for future therapies.

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Mitochondrial Volume Control

Cited by 23 publications

References 69 publications

The Mitochondrial Potassium Cycle

The Mitochondrial Potassium Cycle

Oxidative Stress and Mitochondrial Dysfunction in Cardiovascular Diseases

Prevention of cell damage in ischaemia: novel molecular targets in mitochondria

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