Progression of heart failure is attenuated by antioxidant therapy with N-acetylcysteine in myocardial infarcted female rats

Costa, César Rafael Marins; Seara, Fernando A.C.; Peixoto, Milena Simões; Ramos, Isalira Peroba; Barbosa, Raiana Andrade Quintanilha; Carvalho, Adriana Bastos; Fortunato, Rodrigo S.; Silveira, Anderson Luiz Bezerra da; Olivares, Emerson Lopes

doi:10.1007/s11033-020-05907-4

Cited by 9 publications

(3 citation statements)

References 59 publications

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“…These findings are in consistent with the previous reports. 18,35,36 A major finding of this study is that increased myocyte autophagy in pressure overload-induced heart failure was inhibited by the treatment of antioxidant NAC, as evidenced by decreases in LC3 II expression and the autophagy-related mRNA expression of Atg4b, Atg5, Atg7 and Atg12. In support of our results, other studies have shown that adiponectin ameliorates oxidative stress-induced autophagy in cardiomyocytes.…”

Section: Antioxidants Inhibit Pathological Autophagy and Necroptosis In Myocytes In Pressure Overload-induced Heart Failurementioning

confidence: 75%

Enhanced oxidative stress mediates pathological autophagy and necroptosis in cardiac myocytes in pressure overload induced heart failure in rats

Chi

Wang

et al. 2021

Clin Exp Pharma Physio

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In cardiac myocytes in vitro, hydrogen peroxide induces autophagic cell death and necroptosis. Oxidative stress, myocyte autophagy and necroptosis coexist in heart failure (HF). In this study, we tested the hypothesis that excessive oxidative stress mediates pathological autophagy and necroptosis in myocytes in pressure overloadinduced HF. HF was produced by chronic pressure overload induced by abdominal aortic constriction (AAC) in rats. Rats with AAC or sham operation were randomised to orally receive an antioxidant N-acetylcysteine (NAC) or placebo for 4 weeks.Echocardiography was performed for the assessments of left ventricular (LV) structure and function. AAC rats exhibited decreased LV fractional shortening (FS) at 4 weeks after surgery. NAC treatment attenuated decreased LV FS in AAC rats. In AAC rats, myocardial level of 8-hydroxydeoxyguanosine assessed by immunohistochemical staining, indicative of oxidative stress, was increased, LC3 II protein, a marker of autophagy, Beclin1 protein and Atg4b, Atg5, Atg7 and Atg12 mRNA expression were markedly increased, RIP1, RIP3 and MLKL expression, indicative of necroptosis, was increased, and all of the alterations in AAC rats were prevented by the NAC treatment. NAC treatment also attenuated myocyte cross-sectional area and myocardial fibrosis in AAC rats. In conclusion, NAC treatment prevented the increases in oxidative stress, myocyte autophagy and necroptosis and the decrease in LV systolic function in pressure overload-induced HF. These findings suggest that enhanced oxidative stress mediates pathological autophagy and necroptosis in myocytes, leading to LV systolic dysfunction, and antioxidants may be of value to prevent HF through the inhibition of excessive autophagy and necroptosis.

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Section: Antioxidants Inhibit Pathological Autophagy and Necroptosis In Myocytes In Pressure Overload-induced Heart Failurementioning

confidence: 75%

Enhanced oxidative stress mediates pathological autophagy and necroptosis in cardiac myocytes in pressure overload induced heart failure in rats

Chi

Wang

et al. 2021

Clin Exp Pharma Physio

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“…Another study also demonstrated that NAC protected patients with RP secondary to SSc against DU, although NAC has no significant vasodilator effect on the microcirculation in hands [14]. NAC has been reported to protect against coronary artery diseases (CAD), myocardial infarction (AMI), myocardial injuries, and cardiomyopathy [15][16][17][18][19][20] (Table 2). In patients with cardiac surgery, NAC decreases diabetes-associated cardiovascular, cardiopulmonary bypass, and cardiac surgery complications, including early reperfusion injury, pumpinduced inflammatory response, and myocardial stress [21][22][23].…”

Section: Overview Of Nac and Cardiovascular Diseasesmentioning

confidence: 99%

N-Acetylcysteine and Atherosclerosis: Promises and Challenges

Cui,

Zhu,

Hao

et al. 2023

Antioxidants

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Atherosclerosis remains a leading cause of cardiovascular diseases. Although the mechanism for atherosclerosis is complex and has not been fully understood, inflammation and oxidative stress play a critical role in the development and progression of atherosclerosis. N-acetylcysteine (NAC) has been used as a mucolytic agent and an antidote for acetaminophen overdose with a well-established safety profile. NAC has antioxidant and anti-inflammatory effects through multiple mechanisms, including an increase in the intracellular glutathione level and an attenuation of the nuclear factor kappa-B mediated production of inflammatory cytokines like tumor necrosis factor-alpha and interleukins. Numerous animal studies have demonstrated that NAC significantly decreases the development and progression of atherosclerosis. However, the data on the outcomes of clinical studies in patients with atherosclerosis have been limited and inconsistent. The purpose of this review is to summarize the data on the effect of NAC on atherosclerosis from both pre-clinical and clinical studies and discuss the potential mechanisms of action of NAC on atherosclerosis, as well as challenges in the field.

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“…Study by Xiao et al has demonstrated that in the model of HF, NAC enhanced antioxidant capacity in vivo and reduce cardiomyocyte cell death ( Wu et al, 2014 ). César et al found that treatment with NAC after MI effectively reduced arrhythmia, cardiac remodeling and infarction expansion ( Costa et al, 2020 ). Furthermore, studies by Dilek and Azita et al manifested that NAC significantly alleviated OS and I/R injury in patients with MI, improved left ventricular systolic function and attenuated cardiac remodeling ( Yesilbursa et al, 2006 ; Talasaz et al, 2014 ).…”

Section: Advances In Drug Application To Improve Cardio-cerebrovascular By Interfering Ferroptosismentioning

confidence: 99%

Ferroptosis: New Dawn for Overcoming the Cardio-Cerebrovascular Diseases

Luo

Gong

et al. 2021

Front. Cell Dev. Biol.

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The dynamic balance of cardiomyocytes and neurons is essential to maintain the normal physiological functions of heart and brain. If excessive cells die in tissues, serious Cardio-Cerebrovascular Diseases would occur, namely, hypertension, myocardial infarction, and ischemic stroke. The regulation of cell death plays a role in promoting or alleviating Cardio-Cerebrovascular Diseases. Ferroptosis is an iron-dependent new type of cell death that has been proved to occur in a variety of diseases. In our review, we focus on the critical role of ferroptosis and its regulatory mechanisms involved in Cardio-Cerebrovascular Diseases, and discuss the important function of ferroptosis-related inhibitors in order to propose potential implications for the prevention and treatment of Cardio-Cerebrovascular Diseases.

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Progression of heart failure is attenuated by antioxidant therapy with N-acetylcysteine in myocardial infarcted female rats

Cited by 9 publications

References 59 publications

Enhanced oxidative stress mediates pathological autophagy and necroptosis in cardiac myocytes in pressure overload induced heart failure in rats

Enhanced oxidative stress mediates pathological autophagy and necroptosis in cardiac myocytes in pressure overload induced heart failure in rats

N-Acetylcysteine and Atherosclerosis: Promises and Challenges

Ferroptosis: New Dawn for Overcoming the Cardio-Cerebrovascular Diseases

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