Circadian regulation of kidney function: finding a role for Bmal1

Zhang, Dingguo; Pollock, David M.

doi:10.1152/ajprenal.00580.2017

Cited by 12 publications

(11 citation statements)

References 41 publications

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“…Diurnal potassium rhythm is not well understood, but it has been suggested that the beneficial effects of potassium supplementation on BP were partly due to the resetting of potassium excretion rhythm, especially when the BP rhythm is lost due to salt-sensitive hypertension. 33 This change in diurnal potassium excretion contrasts with the diurnal rhythm of aldosterone excretion that remained intact and in phase with the light–dark cycle. Microarray analysis on mouse kidneys found that the majority of known potassium-regulatory genes were expressed in a circadian-dependent manner, including genes that encode Na + /K + ATPase, H + /K + ATPase, Kir1.3, ROMK, and the BK channel.…”

Section: Discussionmentioning

confidence: 93%

Timing of Food Intake Drives the Circadian Rhythm of Blood Pressure

Zhang¹,

Colson²,

Jin³

et al. 2020

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Timing of food intake has become a critical factor in determining overall cardiometabolic health. We hypothesized that timing of food intake entrains circadian rhythms of blood pressure and renal excretion in mice. Male C57BL/6J mice were fed ad libitum or reverse feeding (RF) where food was available at all times of day or only available during the 12-hour lights-on period, respectively. Mice eating ad libitum had a significantly higher mean arterial pressure (MAP) during lights-off compared to lights-on (113 ± 2 vs 100 ± 2 mmHg, respectively; p < 0.0001); however, RF for 6 days inverted the diurnal rhythm of MAP (99 ± 3 vs 110 ± 3 mmHg, respectively; p < 0.0001). In contrast to MAP, diurnal rhythms of urine volume and sodium excretion remained intact after RF. Male Bmal1 knockout mice (Bmal1KO) underwent the same feeding protocol. As previously reported, Bmal1KO mice did not exhibit a diurnal MAP rhythm during ad libitum feeding (95 ± 1 vs 92 ± 3 mmHg, lights-off vs lights-on; p > 0.05); however, RF induced a diurnal rhythm of MAP (79 ± 3 vs 95 ± 2 mmHg, lights-off vs lights-on phase; p < 0.01). Transgenic PERIOD2::LUCIFERASE knock-in mice were used to assess the rhythm of the clock protein PERIOD2 in ex vivo tissue cultures. The timing of the PER2::LUC rhythm in the renal cortex and suprachiasmatic nucleus was not affected by RF; however, RF induced significant phase shifts in the liver, renal inner medulla and adrenal gland. In conclusion, the timing of food intake controls blood pressure rhythms in mice independent of Bmal1, urine volume or sodium excretion.

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Section: Discussionmentioning

confidence: 93%

Timing of Food Intake Drives the Circadian Rhythm of Blood Pressure

Zhang¹,

Colson²,

Jin³

et al. 2020

Function

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“…BMAL1 is the main transcriptional activator of the circadian clock, which has been shown to regulate the progress of various renal diseases 7–10 . However, researches on its function in renal IRI are limited.…”

Section: Discussionmentioning

confidence: 99%

“…BMAL1 is the main transcriptional activator of the circadian clock, which has been shown to regulate the progress of various renal diseases. 7 , 8 , 9 , 10 However, researches on its function in renal IRI are limited. Previous studies have revealed that the expression level of BMAL1 in cardiac and cerebral tissues decreased significantly after IR, 17 , 28 , 29 which is in line with our study showing that renal IR causes a dramatic decrease in BMAL1 expression level in renal tissues.…”

Section: Discussionmentioning

confidence: 99%

BMAL1 regulates mitochondrial homeostasis in renal ischaemia‐reperfusion injury by mediating the SIRT1/PGC‐1α axis

Huang

et al. 2022

J Cellular Molecular Medi

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The regulation of renal function by circadian gene BMAL1 has been recently recognized; however, the role and mechanism of BMAL1 in renal ischaemia-reperfusion injury (IRI) are still unknown. The purpose of this study was to clarify the pathophysiological role of BMAL1 in renal IRI. We measured the levels of BMAL1 and mitochondrial biogenesis-related proteins, including SIRT1, PGC-1α, NRF1 and TFAM, in rats with renal IRI. In rats, the level of BMAL1 decreased significantly, resulting in inhibition of SIRT1 expression and mitochondrial biogenesis. In addition, under hypoxia and reoxygenation (H/R) stimulation, BMAL1 knockdown decreased the level of SIRT1 and exacerbated the degree of mitochondrial damage and apoptosis.Overexpression of BMAL1 alleviated H/R-induced injury. Furthermore, application of the SIRT1 inhibitor EX527 not only reduced the activities of SIRT1 and PGC-1α but also further aggravated mitochondrial dysfunction and partially reversed the protective effect of BMAL1 overexpression. Moreover, whether in vivo or in vitro, the application of SIRT1 agonist resveratrol rescued the mitochondrial dysfunction caused by H/R or IRI by activating mitochondrial biogenesis. These results indicate that BMAL1 is a key circadian gene that mediates mitochondrial homeostasis in renal IRI through the SIRT1/PGC-1α axis, which provides a new direction for targeted therapy for renal IRI.

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“…Bmal1 stimulates transcription of numerous genes that have been linked to maintaining proper kidney function [25,26]. This relationship has also been shown in kidney-specific knockout mice where Bmal1 was knocked out specifically in renin-producing cells (Renin1dCre-positive).…”

Section: Sodium Handlingmentioning

confidence: 92%