Solute Transport, Energy Consumption, and Production in the Kidney

Sekine, Takashi; Endou, Hitoshi

doi:10.1016/b978-0-12-381462-3.00006-9

Cited by 8 publications

(2 citation statements)

References 246 publications

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“…The S3 segment is the only part of the PT that can selectively undergo glycolysis as well as oxidative phosphorylation, as the S1 and S2 segments are not known to undergo glycolysis (for a review, see Ref. 38). Therefore, the appearance of Muc1 and its role in the upregulation of the glycolytic pathway could potentiate S3 segment recovery after ischemia.…”

Section: Epithelial Hif-1 Mediates Protection and Recovery From Irimentioning

confidence: 98%

Muc1 is protective during kidney ischemia-reperfusion injury

Pastor-Soler

Sutton

Mang

et al. 2015

American Journal of Physiology-Renal Physiology

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Ischemia-reperfusion injury (IRI) due to hypotension is a common cause of human acute kidney injury (AKI). Hypoxia-inducible transcription factors (HIFs) orchestrate a protective response in renal endothelial and epithelial cells in AKI models. As human mucin 1 (MUC1) is induced by hypoxia and enhances HIF-1 activity in cultured epithelial cells, we asked whether mouse mucin 1 (Muc1) regulates HIF-1 activity in kidney tissue during IRI. Whereas Muc1 was localized on the apical surface of the thick ascending limb, distal convoluted tubule, and collecting duct in the kidneys of sham-treated mice, Muc1 appeared in the cytoplasm and nucleus of all tubular epithelia during IRI. Muc1 was induced during IRI, and Muc1 transcripts and protein were also present in recovering proximal tubule cells. Kidney damage was worse and recovery was blocked during IRI in Muc1 knockout mice compared with congenic control mice. Muc1 knockout mice had reduced levels of HIF-1α, reduced or aberrant induction of HIF-1 target genes involved in the shift of glucose metabolism to glycolysis, and prolonged activation of AMP-activated protein kinase, indicating metabolic stress. Muc1 clearly plays a significant role in enhancing the HIF protective pathway during ischemic insult and recovery in kidney epithelia, providing a new target for developing therapies to treat AKI. Moreover, our data support a role specifically for HIF-1 in epithelial protection of the kidney during IRI as Muc1 is present only in tubule epithelial cells.

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Section: Epithelial Hif-1 Mediates Protection and Recovery From Irimentioning

confidence: 98%

Muc1 is protective during kidney ischemia-reperfusion injury

Pastor-Soler

Sutton

Mang

et al. 2015

American Journal of Physiology-Renal Physiology

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“…The lack of change in S4o in CI-linked respiration implies that the leak of respiration, mitochondrial processes that consume ∆Ψm without contributing to ATP production [25], are not significantly affected in the time interval evaluated, which explain the maintain of mitochondrial coupling in CI-linked respiration ( Figure 3B). On the other hand, mitochondrial ATP production in high energy demanding segments like the proximal tubule (PT) is principally sustained by β-oxidation of FA, like palmitate that represents ~25% of total FAs in plasma [26]. Likewise, proteomic and Western blot analysis of the remnant kidney in 5/6Nx rats shows a reduction in FA β-oxidation-related proteins on day 28 [22] and we recently reported in a model of kidney damage induced by folic acid, that the impairment in OXPHOS capacity and the decrease in β-oxidation favor the transition from AKI to CKD [10].…”

Section: /6nx Induces a Permanent Decrease In Oxidative Phosphorylatmentioning

confidence: 99%

Temporal Alterations in Mitochondrial β-Oxidation and Oxidative Stress Aggravate Chronic Kidney Disease Development in 5/6 Nephrectomy Induced Renal Damage

Aparicio-Trejo

Rojas-Morales

Avila-Rojas

et al. 2020

IJMS

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Five-sixths nephrectomy (5/6Nx) model is widely used for studying the mechanisms involved in chronic kidney disease (CKD) progression, a kidney pathology that has increased dramatically in recent years. Mitochondrial impairment is a key mechanism that aggravates CKD progression; however, the information on mitochondrial bioenergetics and redox alterations along a time course in a 5/6Nx model is still limited and in some cases contradictory. Therefore, we performed for the first time a time-course study of mitochondrial alterations by high-resolution respirometry in the 5/6Nx model. Our results show a decrease in mitochondrial β-oxidation at early times, as well as a permanent impairment in adenosine triphosphate (ATP) production in CI-linked respiration, a permanent oxidative state in mitochondria and decoupling of these organelles. These pathological alterations are linked to the early decrease in complex I and ATP synthase activities and to the further decrease in complex III activity. Therefore, our results may suggest that mitochondrial bioenergetics impairment is an early event in renal damage, whose persistence in time aggravates CKD development in the 5/6Nx model.

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