Expanding Saga of the Renin-Angiotensin System

Jugdutt, Bodh I.

doi:10.1161/circulationaha.115.016328

Cited by 13 publications

(11 citation statements)

References 19 publications

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“…The activation of the renin-angiotensin-aldosterone (Aldo) system (RAAS) plays a pivotal role in patients with hypertension [1], diabetes and other progressive nephropathies [2,3] and may cause various physiological effects through both genomic and non-genomic mechanisms [4]. Although interruption of the RAAS by angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) significantly reduces morbidity and mortality [5,6] as well as the severity of proteinuria and nephrology in patients with chronic kidney disease (CKD) [7,8], Aldo concentrations 'escape' to baseline during longterm therapy [9].…”

Section: Introductionmentioning

confidence: 99%

Berberine Improved Aldo-Induced Podocyte Injury via Inhibiting Oxidative Stress and Endoplasmic Reticulum Stress Pathways both In Vivo and In Vitro

Wang¹,

Xu²,

He³

et al. 2016

Cell Physiol Biochem

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Background/Aims: Berberine, a naturally occurring isoquinoline alkaloid, acts against oxidative stress (OS) and endoplasmic reticulum stress (ERS), both of which are responsible for Aldosterone (Aldo) -induced podocyte injury. However, the direct effects of berberine on Aldo-induced OS, ERS, and podocyte injury are not well defined. Methods: Uninephrectomized Sprague-Dawley rats were given 1% NaCl (salt) in their water and an Aldo infusion (0.75 µg/h) for 28 days to induce podocyte injury in the Aldo group. In the Aldo/berberine group, in addition to Aldo infusion, rats were administered 150 mg/kg berberine per day by gastric gavage for 4 weeks. Podocytes were incubated in media containing either buffer or Aldo in the presence or absence of berberine for variable time periods. The kidney tissues and podocytes were then investigated using morphological analysis, immunohistochemistry, transmission electron microscopy, western blot, DHE staining, DCFDA fluorescence, and Annexin V staining. Results: Here, we have reported that berberine attenuated Aldo-induced OS, ERS, and podocyte injury both in vivo and in vitro. Additionally, berberine treatment improved the extensive fusion of foot processes in electron micrographs resulting from Aldo/salt infusion in rats. Conclusion: Berberine may be examined as an effective agent against Aldo-induced podocyte injury.

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Section: Introductionmentioning

confidence: 99%

Berberine Improved Aldo-Induced Podocyte Injury via Inhibiting Oxidative Stress and Endoplasmic Reticulum Stress Pathways both In Vivo and In Vitro

Wang¹,

Xu²,

He³

et al. 2016

Cell Physiol Biochem

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“…As a critical mediator of the RAAS, plasma and tissue Aldo levels are elevated in patients with hypertension (21), and diabetic and other progressive nephropathies (22,23), and may exert various physiological effects (24). Although interruption of the RAAS with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers significantly improves kidney injury, Aldo concentrations ‘escape’ to baseline during chronic therapy (25).…”

Section: Discussionmentioning

confidence: 99%

Autophagy is involved in aldosterone-induced mesangial cell proliferation

Wang

Miao

et al. 2016

Molecular Medicine Reports

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The aim of the present study was to investigate whether autophagy is involved in aldosterone (Aldo)-induced mesangial cell (MC) proliferation. MCs were incubated with 10−7 M Aldo for 24 h. Proliferation of MCs, and the underlying mechanisms, were subsequently analyzed using [3H]thymidine assay, cell counting assay, western blotting and RNA interference (RNAi). Aldo was revealed to induce autophagy, as indicated by the increased conversion from microtubule-associated protein 1A/1B-light chain 3 (LC3)-I to LC3-II, the increased expression levels of autophagy-related gene 7 (Atg7) and the increased degradation of p62, which was accompanied by MC proliferation. Notably, pharmacological inhibition of autophagy or RNAi-mediated knockdown of Atg7 attenuated Aldo-induced MC proliferation, suggesting that autophagy was at least partially responsible for this effect. The results of the present study provided evidence that autophagy is critical for regulating Aldo-induced MC proliferation.

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“…Renin release is regulated by an intrarenal baroreceptor that detects pressure in the afferent arteriole, by β-adrenergic sympathetic innervation and the delivery of salt (especially Cl) in the tubular fluid. 17 , 18 , 20 …”

Section: Renin-angiotensin Aldosterone System and Hypertensionmentioning

confidence: 99%

The role of renin-angiotensin aldosterone system related micro-ribonucleic acids in hypertension

Wang

Yang

2015

SMJ

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Micro-ribonucleic acids (miRNAs) are small (21-25 nucleotide) single-stranded, evolutionarily conserved non-protein-coding RNAs, which control diverse cellular functions by interacting with the 3’ untranslated region of specific target messenger RNAs at the post-transcriptional level. Research shows that an aberrant expression profile of miRNAs has been linked to a series of diseases, including hypertension. In the past few decades, it has been demonstrated that excessive activation of the renin-angiotensin aldosterone system (RAAS) involves in the pathogenesis of hypertension. This article reviews the latest insights in the identification of RAAS-correlative miRNAs and the potential mechanisms for their roles in hypertension.

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Expanding Saga of the Renin-Angiotensin System

Cited by 13 publications

References 19 publications

Berberine Improved Aldo-Induced Podocyte Injury via Inhibiting Oxidative Stress and Endoplasmic Reticulum Stress Pathways both In Vivo and In Vitro

Berberine Improved Aldo-Induced Podocyte Injury via Inhibiting Oxidative Stress and Endoplasmic Reticulum Stress Pathways both In Vivo and In Vitro

Autophagy is involved in aldosterone-induced mesangial cell proliferation

The role of renin-angiotensin aldosterone system related micro-ribonucleic acids in hypertension

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