Mitochondria–Power Players in Kidney Function?

Forbes, Josephine M.

doi:10.1016/j.tem.2016.05.002

Cited by 87 publications

(69 citation statements)

References 10 publications

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“…These findings could generally be associated with regulating energy utilization because the kidneys are second only to the heart in mitochondrial abundance and oxygen consumption, 53 and because the RPTCs constitute approximately half of the kidney mass and use the majority of oxygen consumed by the organ. 54 A link between mitochondrial morphology and bioenergetics was first reported decades ago, 55 with a substantial amount of supporting data accumulating ever since. The relationship between the two mitochondrial features is reciprocal, as evident from studies showing that manipulation of mitochondrial dynamics led to deficiencies in mitochondrial respiration and ATP depletion.…”

Section: Disscussionmentioning

confidence: 95%

“…The current work further highlights the contribution of CB 1 R‐induced mitochondrial fragmentation to such cellular damage. These findings could generally be associated with regulating energy utilization because the kidneys are second only to the heart in mitochondrial abundance and oxygen consumption, and because the RPTCs constitute approximately half of the kidney mass and use the majority of oxygen consumed by the organ …”

Section: Disscussionmentioning

confidence: 99%

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Cannabinoid‐1 receptor regulates mitochondrial dynamics and function in renal proximal tubular cells

Drori

Permyakova

Hadar

et al. 2018

Diabetes Obesity Metabolism

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Section: Disscussionmentioning

confidence: 95%

Section: Disscussionmentioning

confidence: 99%

Cannabinoid‐1 receptor regulates mitochondrial dynamics and function in renal proximal tubular cells

Drori

Permyakova

Hadar

et al. 2018

Diabetes Obesity Metabolism

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“…Fatty acids are then broken down for energy via β-oxidation in the mitochondrial matrix. Although β-oxidation is the most efficient mechanism for producing ATP in proximal tubules, it is important to note that due to the high consumption of oxygen by proximal tubules, they are more susceptible than other cell types to changes in oxygen levels 20,21 . A decrease in oxygen levels can lead to impaired β-oxidation and a reduction in ATP production (see below).…”

Section: Mitochondrial Functionmentioning

confidence: 99%

Mitochondrial energetics in the kidney

2017

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The kidney requires a large number of mitochondria to remove waste from the blood and regulate fluid and electrolyte balance. Mitochondria provide the energy to drive these important functions and can adapt to different metabolic conditions through a number of signalling pathways (for example, mechanistic target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK) pathways) that activate the transcriptional co-activator peroxisome proliferator-activated receptor-γ co-activator 1α (PGC1α), and by balancing mitochondrial dynamics and energetics to maintain mitochondrial homeostasis. Mitochondrial dysfunction leads to a decrease in ATP production, alterations in cellular functions and structure, and the loss of renal function. Persistent mitochondrial dysfunction has a role in the early stages and progression of renal diseases, such as acute kidney injury (AKI) and diabetic nephropathy, as it disrupts mitochondrial homeostasis and thus normal kidney function. Improving mitochondrial homeostasis and function has the potential to restore renal function, and administering compounds that stimulate mitochondrial biogenesis can restore mitochondrial and renal function in mouse models of AKI and diabetes mellitus. Furthermore, inhibiting the fission protein dynamin 1-like protein (DRP1) might ameliorate ischaemic renal injury by blocking mitochondrial fission.

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“…Consistent with these key roles of NAD + , various cardiac and renal stresses have been associated with decreases in the levels of this metabolite, which contribute to disease pathogenesis 1,5 . Acute stresses, such as stroke, myocardial infarction, acute kidney injury (AKI) and ischaemia, deplete cellular NAD + levels and reduce NAD + synthesis 5,6 .…”

mentioning

confidence: 82%

“…The heart and kidneys have the highest numbers of mitochondria and are among the greatest oxygen consumers of all organs in the body 1 . Energy production is maintained in these organs through the oxidative metabolism of a range of fuels.…”

mentioning

confidence: 99%

Role of NAD+ and mitochondrial sirtuins in cardiac and renal diseases

2017

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The coenzyme nicotinamide adenine dinucleotide (NAD+) has key roles in the regulation of redox status and energy metabolism. NAD+ depletion is emerging as a major contributor to the pathogenesis of cardiac and renal diseases and NAD+ repletion strategies have shown therapeutic potential as a means to restore healthy metabolism and physiological function. The pleotropic roles of NAD+ enable several possible avenues by which repletion of this coenzyme could have therapeutic efficacy. In particular, NAD+ functions as a co-substrate in deacylation reactions carried out by the sirtuin family of enzymes. These NAD+-dependent deacylases control several aspects of metabolism and a wealth of data suggests that boosting sirtuin activity via NAD+ supplementation might be a promising therapy for cardiac and renal pathologies. This Review summarizes the role of NAD+ metabolism in the heart and kidney, and highlights the mitochondrial sirtuins as mediators of some of the beneficial effects of NAD+-boosting therapies in preclinical animal models. We surmise that modulating the NAD+–sirtuin axis is a clinically relevant approach to develop new therapies for cardiac and renal diseases.

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Mitochondria–Power Players in Kidney Function?

Cited by 87 publications

References 10 publications

Cannabinoid‐1 receptor regulates mitochondrial dynamics and function in renal proximal tubular cells

Cannabinoid‐1 receptor regulates mitochondrial dynamics and function in renal proximal tubular cells

Mitochondrial energetics in the kidney

Role of NAD+ and mitochondrial sirtuins in cardiac and renal diseases

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