Activation of Mas and pGCA receptor pathways protects renal epithelial cell damage against oxidative-stress-induced injury

Ghatage, Trupti; Singh, Sameer; Mandal, Kalyaneswar; Jadhav, Kirtikumar B.; Dhar, Animesh

doi:10.1016/j.peptides.2023.170959

Cited by 3 publications

(3 citation statements)

References 31 publications

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“…Natriuretic peptides, particularly the atrial natriuretic peptide (ANP), are also known to have important vasodilatory and anti-hypertensive properties [98]. Recent evidence reported a strong protective effect of a novel dual-acting peptide (DAP) against vascular damage: this peptide, combining the Ang 1-7 sequence with part of the brain natriuretic peptide (BNP) and of ANP, enhances the cardiovascular protection provided by the single elements, acting via the co-activation of Mas and particulate guanylyl cyclase-A receptor, reducing H 2 O 2 -induced ROS generation, preventing vascular hypertrophy, attenuating intracellular calcium levels (and therefore, contraction) in VSMC and activating PI3K/AKT/eNOS pathway in ECs [99,100].…”

Section: Endothelial and Vascular Damagementioning

confidence: 99%

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The RAAS Goodfellas in Cardiovascular System

Caputo,

Bertoldi,

Driussi

et al. 2023

JCM

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In the last two decades, the study of the renin–angiotensin–aldosterone system (RAAS) has revealed a counterregulatory protective axis. This protective arm is characterized by ACE2/Ang 1-7/MasR and Ang 1-9 that largely counteracts the classic arm of the RAAS mediated by ACE/Ang II/AT1R/aldosterone and plays an important role in the prevention of inflammation, oxidative stress, hypertension, and cardiovascular remodeling. A growing body of evidence suggests that enhancement of this counterregulatory arm of RAAS represents an important therapeutic approach to facing cardiovascular comorbidities. In this review, we provide an overview of the beneficial effects of ACE2, Ang 1-7/MasR, and Ang 1-9 in the context of oxidative stress, vascular dysfunction, and organ damage.

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Section: Endothelial and Vascular Damagementioning

confidence: 99%

“…Combining Ang 1-7 with natriuretic peptides, Ghatage and coworkers created a dual activating peptide (DAP) that, activating both Mas and pGCA receptor, plays a beneficial role in cultured renal tubular NRK-52E epithelial cells, by decreasing the pro-oxidative and pro-inflammatory environment induced by H 2 O 2 [100].…”

Section: Kidneymentioning

confidence: 99%

The RAAS Goodfellas in Cardiovascular System

Caputo,

Bertoldi,

Driussi

et al. 2023

JCM

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“…[20] Recent studies have confirmed the anti-inflammatory and anti-OS properties in acute lung injury, cardiovascular diseases, renal injury, and osteoarthritis. [21][22][23][24] Meng et al found that Nesfatin-1 inhibits endothelial inflammation and OS through the Gfi1/nuclear factor-κB (NF-κB) signaling pathway. [25] Additionally, Gharanei found that Nesfatin-1 reduces inflammation in mice white adipose tissue through NUCB2/NF-kB pathways.…”

Section: Introductionmentioning

confidence: 99%

Nesfatin‐1 alleviates hyperoxia‐induced bronchopulmonary dysplasia (BPD) via the nuclear factor‐κB (NF‐κB) p65 signaling pathway

Zhang,

Zhuo,

Chen

et al. 2024

J Biochem & Molecular Tox

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Bronchopulmonary dysplasia (BPD) is a chronic respiratory disease in newborns, which severely influences the health of infants and lacks effective clinical treatment strategies. The pathogenesis of BPD is correlated to enhanced inflammation and activated oxidative stress (OS). The application of antioxidants and anti‐inflammatory treatment could be hot spots for BPD treatment. Nesfatin‐1, a peptide with a suppressive property against inflammation, was tested herein for its potential therapeutic value in BPD. Neonatal SD rats were stimulated with hyperoxia, followed by being intraperitoneally administered with 20 μg/kg/day Nesfatin‐1 for 2 weeks. Decreased RAC value in lung tissues, increased wet weight/dry weight (W/D) pulmonary ratio and bronchoalveolar lavage fluid (BALF) proteins, elevated cytokine release in BALF, increased malondialdehyde (MDA) content, and declined superoxide dismutase (SOD) activity were observed in BPD rats, all of which were sharply mitigated by Nesfatin‐1. Rat epithelial type II cells (AECIIs) were handled with hyperoxia, and then cultured with 1 and 10 nM Nesfatin‐1. Reduced cell viability, elevated lactate dehydrogenase production, elevated cytokine secretion, elevated MDA content, and decreased SOD activity were observed in hyperoxia‐handled AECIIs, all of which were markedly alleviated by Nesfatin‐1. Furthermore, activated nuclear factor‐κB (NF‐κB) signaling observed in both BPD rats and hyperoxia‐handled AECIIs were notably repressed by Nesfatin‐1. Collectively, Nesfatin‐1 alleviated hyperoxia‐triggered BPD by repressing inflammation and OS via the NF‐κB signaling pathway.

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