Test Driving Levosimendan as the New “Kidney Protector”

Gamilla-Crudo, Ann Kathleen; Kadambi, Pradeep V.; Prough, Donald S.

doi:10.1097/ccm.0b013e3182963fdc

Cited by 3 publications

(1 citation statement)

References 17 publications

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“…It has renoprotective effect after cardiopulmonary bypass surgery. 100 The molecular mechanism of levosimendan-evoked protection might include an interaction with mitochondrial energy conservation through mitochondrial ATP-sensitive K 1 channels. A clinical study of levosimendan, investigating the safety and efficacy in intensive care patients with AKI, is now ongoing (clinicaltrials.gov identifier NCT01720030).…”

Section: Targeting Mitochondrial Biogenesismentioning

confidence: 99%

Mitochondria in Sepsis-Induced AKI

Sun

Zhang

Tian

et al. 2019

JASN

185

119

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AKI is a common clinical condition associated with the risk of developing CKD and ESKD. Sepsis is the leading cause of AKI in the intensive care unit (ICU) and accounts for nearly half of all AKI events. Patients with AKI who require dialysis have an unacceptably high mortality rate of 60%–80%. During sepsis, endothelial activation, increased microvascular permeability, changes in regional blood flow distribution with resulting areas of hypoperfusion, and hypoxemia can lead to AKI. No effective drugs to prevent or treat human sepsis-induced AKI are currently available. Recent research has identified dysfunction in energy metabolism as a critical contributor to the pathogenesis of AKI. Mitochondria, the center of energy metabolism, are increasingly recognized to be involved in the pathophysiology of sepsis-induced AKI and mitochondria could serve as a potential therapeutic target. In this review, we summarize the potential role of mitochondria in sepsis-induced AKI and identify future therapeutic approaches that target mitochondrial function in an effort to treat sepsis-induced AKI.

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Section: Targeting Mitochondrial Biogenesismentioning

confidence: 99%

Mitochondria in Sepsis-Induced AKI

Sun

Zhang

Tian

et al. 2019

JASN

185

119

View full text Add to dashboard Cite

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Levosimendan: A New Therapeutical Strategy in Patients with Renal Insufficiency

Liu,

Lu,

et al. 2024

Cardiovasc Drugs Ther

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Mitochondria: a therapeutic target in acute kidney injury

Ishimoto

Inagi

2015

Nephrol. Dial. Transplant.

159

148

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Acute kidney injury (AKI) is a common clinical entity that is associated with high mortality and morbidity. It is a risk factor for the development and progression of chronic kidney disease. Presently, no effective treatment for AKI is available, and novel therapeutic approaches are desperately needed. Accumulating evidence highlights mitochondrial dysfunction as an important factor in the pathogenesis of AKI. Recent advances in our understanding of the molecules involved in mitochondrial biogenesis, fusion/fission, mitophagy and their pathophysiological roles will lead to the development of drugs that target mitochondria for the treatment of various diseases, including AKI. In this review, we summarize current knowledge of the contribution of mitochondria-related pathophysiology in AKI and the prospective benefits of mitochondria-targeting therapeutic approaches against AKI.

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Test Driving Levosimendan as the New “Kidney Protector”

Cited by 3 publications

References 17 publications

Mitochondria in Sepsis-Induced AKI

Mitochondria in Sepsis-Induced AKI

Levosimendan: A New Therapeutical Strategy in Patients with Renal Insufficiency

Mitochondria: a therapeutic target in acute kidney injury

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