Epigallocatechin-3-Gallate Inhibits Atrial Fibrosis and Reduces the Occurrence and Maintenance of Atrial Fibrillation and its Possible Mechanisms

Li, Tao; Tong, Qi; Wang, Zhengjie; Yang, Ziqi; Sun, Yiren; Cai, Jie; Xu, Qiyue; Lu, Yuan; Liu, Xuemei; Lin, Ke; Qian, Yongjun

doi:10.1007/s10557-023-07447-y

Cited by 3 publications

(2 citation statements)

References 66 publications

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“…For the Ang II and Ang II + ANP groups, osmotic mini-pumps containing Ang II (MedChemExpress, Monmouth, NJ) were used to infuse at a rate of 1 µg/kg/min for the same duration. The Ang II + ANP and ANP groups received mini-pumps filled with carperitide, a recombinant α-human ANP (MedChemExpress, State of New Jersey, USA), dissolved in distilled water and released at a rate of 0.1 µg/kg/min over 14 days, connected to the right or left jugular vein using a small polyethylene catheter [ 19 – 20 ]. Rat weights were systematically documented on days 0, 7, and 14, and systolic blood pressure was measured on these days using a tail-cuff method without anesthesia.…”

Section: Methodsmentioning

confidence: 99%

Targeting myocardial inflammation: investigating the therapeutic potential of atrial natriuretic peptide in atrial fibrosis

Zhu,

Li,

Bai

et al. 2024

Mol Biol Rep

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Background Atrial Fibrillation (AF), a prevalent arrhythmic condition, is intricately associated with atrial fibrosis, a major pathological contributor. Central to the development of atrial fibrosis is myocardial inflammation. This study focuses on Atrial Natriuretic Peptide (ANP) and its role in mitigating atrial fibrosis, aiming to elucidate the specific mechanisms by which ANP exerts its effects, with an emphasis on fibroblast dynamics. Methods and results The study involved forty Sprague-Dawley rats, divided into four groups: control, Angiotensin II (Ang II), Ang II + ANP, and ANP only. The administration of 1 µg/kg/min Ang II was given to Ang II and Ang II + ANP groups, while both Ang II + ANP and ANP groups received 0.1 µg/kg/min ANP intravenously for a duration of 14 days. Cardiac fibroblasts were used for in vitro validation of the proposed mechanisms. The study observed that rats in the Ang II and Ang II + ANP groups showed an increase in blood pressure and a decrease in body weight, more pronounced in the Ang II group. Diastolic dysfunction, a characteristic of the Ang II group, was alleviated by ANP. Additionally, ANP significantly reduced Ang II-induced atrial fibrosis, myofibroblast proliferation, collagen overexpression, macrophage infiltration, and the elevated expression of Interleukin 6 (IL-6) and Tenascin-C (TN-C). Transcriptomic sequencing indicated enhanced PI3K/Akt signaling in the Ang II group. Furthermore, in vitro studies showed that ANP, along with the PI3K inhibitor LY294002, effectively reduced PI3K/Akt pathway activation and the expression of TN-C, collagen-I, and collagen-III, which were induced by Ang II. Conclusions The study demonstrates ANP’s potential in inhibiting myocardial inflammation and reducing atrial fibrosis. Notably, ANP’s effect in countering atrial fibrosis seems to be mediated through the suppression of the Ang II-induced PI3K/Akt-Tenascin-C signaling pathway. These insights enhance our understanding of AF pathogenesis and position ANP as a potential therapeutic agent for treating atrial fibrosis.

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Section: Methodsmentioning

confidence: 99%

Targeting myocardial inflammation: investigating the therapeutic potential of atrial natriuretic peptide in atrial fibrosis

Zhu,

Li,

Bai

et al. 2024

Mol Biol Rep

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“…These studies also illustrated that EGCG altered the activation of JNK, Akt and β-catenin but interestingly not the Smad2/3 pathway. In contrast, the application of EGCG in a rat model of atrial fibrosis resulted in attenuated Smad2/3 activation in addition to diminished fibrosis and expression of collagens type I and III [ 82 ]. EGCG also attenuated lysyl oxidase expression, an enzyme involved in cross-linking of ECM proteins collagen and fibronectin.…”

Section: Major Plant-derived Compounds That Modulate Fibrosismentioning

confidence: 99%

Potential of Plant-Derived Compounds in Preventing and Reversing Organ Fibrosis and the Underlying Mechanisms

Azeredo,

Fan,

Murphy

et al. 2024

Cells

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Increased production of extracellular matrix is a necessary response to tissue damage and stress. In a normal healing process, the increase in extracellular matrix is transient. In some instances; however, the increase in extracellular matrix can persist as fibrosis, leading to deleterious alterations in organ structure, biomechanical properties, and function. Indeed, fibrosis is now appreciated to be an important cause of mortality and morbidity. Extensive research has illustrated that fibrosis can be slowed, arrested or even reversed; however, few drugs have been approved specifically for anti-fibrotic treatment. This is in part due to the complex pathways responsible for fibrogenesis and the undesirable side effects of drugs targeting these pathways. Natural products have been utilized for thousands of years as a major component of traditional medicine and currently account for almost one-third of drugs used clinically worldwide. A variety of plant-derived compounds have been demonstrated to have preventative or even reversal effects on fibrosis. This review will discuss the effects and the underlying mechanisms of some of the major plant-derived compounds that have been identified to impact fibrosis.

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Ferroptosis: Latest evidence and perspectives on plant‐derived natural active compounds mitigating doxorubicin‐induced cardiotoxicity

Wang,

Liu

et al. 2024

J of Applied Toxicology

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Doxorubicin (DOX) is a chemotherapy drug widely used in clinical settings, acting as a first‐line treatment for various malignant tumors. However, its use is greatly limited by the cardiotoxicity it induces, including doxorubicin‐induced cardiomyopathy (DIC). The mechanisms behind DIC are not fully understood, but its potential biological mechanisms are thought to include oxidative stress, inflammation, energy metabolism disorders, mitochondrial damage, autophagy, apoptosis, and ferroptosis. Recent studies have shown that cardiac injury induced by DOX is closely related to ferroptosis. Due to their high efficacy, availability, and low side effects, natural medicine treatments hold strong clinical potential. Currently, natural medicines have been shown to mitigate DOX‐induced ferroptosis and ease DIC through various functions such as antioxidation, iron ion homeostasis correction, lipid metabolism regulation, and mitochondrial function improvement. Therefore, this review summarizes the mechanisms of ferroptosis in DIC and the regulation by natural plant products, with the expectation of providing a reference for future research and development of inhibitors targeting ferroptosis in DIC.This review explores the mechanisms of ferroptosis in doxorubicin‐induced cardiomyopathy (DIC) and summarizes how natural plant products can alleviate DIC by inhibiting ferroptosis through reducing oxidative stress, correcting iron ion homeostasis, regulating lipid metabolism, and improving mitochondrial function.

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Epigallocatechin-3-Gallate Inhibits Atrial Fibrosis and Reduces the Occurrence and Maintenance of Atrial Fibrillation and its Possible Mechanisms

Cited by 3 publications

References 66 publications

Targeting myocardial inflammation: investigating the therapeutic potential of atrial natriuretic peptide in atrial fibrosis

Targeting myocardial inflammation: investigating the therapeutic potential of atrial natriuretic peptide in atrial fibrosis

Potential of Plant-Derived Compounds in Preventing and Reversing Organ Fibrosis and the Underlying Mechanisms

Ferroptosis: Latest evidence and perspectives on plant‐derived natural active compounds mitigating doxorubicin‐induced cardiotoxicity

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