Sesamin suppresses <scp>angiotensin‐II</scp>‐enhanced oxidative stress and hypertrophic markers in H9c2 cells

Chang, Chih-Chia; Cheng, Hui-Ching; Chou, Wan-Ching; Huang, Yu‐Ting; Hsieh, Pei‐Ling; Chu, Pei Yi; Lee, Shin-Da

doi:10.1002/tox.23853

Cited by 4 publications

(4 citation statements)

References 41 publications

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“…Both systemic and local RAS act mutually in different tissues 32 . Importantly, the upregulation of AngII and activation of AT1 trigger the development of oxidative stress and inflammation by activating NADPH oxidase and inducing mitochondrial dysfunction 33 . Notably, NADPH oxidase is upregulated during the aging process and aging‐related disorders such as diabetes, hypertension, and atherosclerosis.…”

Section: A Brief Overview Of Rasmentioning

confidence: 99%

“… 32 Importantly, the upregulation of AngII and activation of AT1 trigger the development of oxidative stress and inflammation by activating NADPH oxidase and inducing mitochondrial dysfunction. 33 Notably, NADPH oxidase is upregulated during the aging process and aging‐related disorders such as diabetes, hypertension, and atherosclerosis. However, stimulation of AT2 by AngII leads to an opposing effect characterized by inhibition of inflammation and oxidative stress mediated by AT1.…”

Section: A Brief Overview Of Rasmentioning

confidence: 99%

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Role of brain renin–angiotensin system in depression: A new perspective

Ali,

Al‐Kuraishy,

Al‐Gareeb

et al. 2023

CNS Neurosci Ther

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Depression is a mood disorder characterized by abnormal thoughts. The pathophysiology of depression is related to the deficiency of serotonin (5HT), which is derived from tryptophan (Trp). Mitochondrial dysfunction, oxidative stress, and neuroinflammation are involved in the pathogenesis of depression. Notably, the renin–angiotensin system (RAS) is involved in the pathogenesis of depression, and different findings revealed that angiotensin‐converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) may be effective in depression. However, the underlying mechanism for the role of dysregulated brain RAS‐induced depression remains speculative. Therefore, this review aimed to revise the conceivable role of ACEIs and ARBs and how these agents ameliorate the pathophysiology of depression. Dysregulation of brain RAS triggers the development and progression of depression through the reduction of brain 5HT and expression of brain‐derived neurotrophic factor (BDNF) and the induction of mitochondrial dysfunction, oxidative stress, and neuroinflammation. Therefore, inhibition of central classical RAS by ARBS and ACEIs and activation of non‐classical RAS prevent the development of depression by regulating 5HT, BDNF, mitochondrial dysfunction, oxidative stress, and neuroinflammation.

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Section: A Brief Overview Of Rasmentioning

confidence: 99%

Section: A Brief Overview Of Rasmentioning

confidence: 99%

Role of brain renin–angiotensin system in depression: A new perspective

Ali,

Al‐Kuraishy,

Al‐Gareeb

et al. 2023

CNS Neurosci Ther

View full text Add to dashboard Cite

show abstract

“… 29 Moreover, the RAS can induce paracrine and autocrine effects regardless of its systemic effects. 30 The harmful effect of AngII such as oxidative stress, mitochondrial dysfunction and inflammation is mediated through activation of NADPH oxidase. 26 It has been revealed that exaggerated NADPH oxidase activity and associated oxidative stress is linked with the development of age‐related disorders such as PD.…”

Section: Overview Of Rasmentioning

confidence: 99%

The potential role of brain renin‐angiotensin system in the neuropathology of Parkinson disease: Friend, foe or turncoat?

Al‐Qahtani,

Al‐kuraishy,

Al‐Gareeb

et al. 2024

J Cellular Molecular Medi

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Parkinson disease (PD) is one of the most common neurodegenerative diseases of the brain. Of note, brain renin‐angiotensin system (RAS) is intricate in the PD neuropathology through modulation of oxidative stress, mitochondrial dysfunction and neuroinflammation. Therefore, modulation of brain RAS by angiotensin receptor blockers (ARBs) and angiotensin‐converting enzyme inhibitors (ACEIs) may be effective in reducing the risk and PD neuropathology. It has been shown that all components including the peptides and enzymes of the RAS are present in the different brain areas. Brain RAS plays a critical role in the regulation of memory and cognitive function, and in the controlling of central blood pressure. However, exaggerated brain RAS is implicated in the pathogenesis of different neurodegenerative diseases including PD. Two well‐known pathways of brain RAS are recognized including; the classical pathway which is mainly mediated by AngII/AT1R has detrimental effects. Conversely, the non‐classical pathway which is mostly mediated by ACE2/Ang1‐7/MASR and AngII/AT2R has beneficial effects against PD neuropathology. Exaggerated brain RAS affects the viability of dopaminergic neurons. However, the fundamental mechanism of brain RAS in PD neuropathology was not fully elucidated. Consequently, the purpose of this review is to disclose the mechanistic role of RAS in in the pathogenesis of PD. In addition, we try to revise how the ACEIs and ARBs can be developed for therapeutics in PD.

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“…There has been recent interest in the ability of certain natural compounds to affect upstream signaling pathways that modulate the immune response, and hence potentially prevent cardiac hypertrophy. 10,11 The CTRP3 is a member of C1q/tumor necrosis factor (TNF)-related proteins and is widely expressed in different tissues, such as white adipose tissue, fibroblasts, chondrocytes, and monocytes. 12,13 It possesses multiple biological functions, such as regulating adipokine secretion, 14 promoting cell proliferation, 15 regulating hepatic lipid metabolism, 16 and inhibiting the inflammatory response.…”

Section: Introductionmentioning

confidence: 99%