The cardioprotective effects of hydrogen sulfide by targeting endoplasmic reticulum stress and the Nrf2 signaling pathway: A review

Yarmohammadi, Fatemeh; Hayes, A. Wallace; Karimi, Gholamreza

doi:10.1002/biof.1763

Cited by 17 publications

(8 citation statements)

References 106 publications

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“…Once regarded as merely a toxic and foul-smelling gas, H 2 S has more recently been recognized as a key signaling molecule and important endogenous mediator of numerous physiological and pathophysiological processes within mammalian systems. Its positive influence on the cardiovascular system, in particular, is rooted in its involvement in vasodilation (activation of K ATP channels and the PI3K/Akt signaling pathway) [ 178 , 179 , 180 , 181 ], as well as its anti-inflammatory (inhibition of the p38 MAPK/NF-κB pathway) [ 182 , 183 ], antioxidative (activation of the Nrf2 signaling pathway) [ 59 , 168 , 184 ], and anti-apoptotic (suppression of pro-apoptotic genes Bid, Apaf-1, and p53) [ 140 ] properties, which have been extensively reviewed elsewhere in the literature [ 54 , 55 , 116 , 185 ].…”

Section: Discussionmentioning

confidence: 99%

H2S Donors with Cytoprotective Effects in Models of MI/R Injury and Chemotherapy-Induced Cardiotoxicity

Lukesh

2023

Antioxidants

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Hydrogen sulfide (H2S) is an endogenous signaling molecule that greatly influences several important (patho)physiological processes related to cardiovascular health and disease, including vasodilation, angiogenesis, inflammation, and cellular redox homeostasis. Consequently, H2S supplementation is an emerging area of interest, especially for the treatment of cardiovascular-related diseases. To fully unlock the medicinal properties of hydrogen sulfide, however, the development and refinement of H2S releasing compounds (or donors) are required to augment its bioavailability and to better mimic its natural enzymatic production. Categorizing donors by the biological stimulus that triggers their H2S release, this review highlights the fundamental chemistry and releasing mechanisms of a range of H2S donors that have exhibited promising protective effects in models of myocardial ischemia-reperfusion (MI/R) injury and cancer chemotherapy-induced cardiotoxicity, specifically. Thus, in addition to serving as important investigative tools that further advance our knowledge and understanding of H2S chemical biology, the compounds highlighted in this review have the potential to serve as vital therapeutic agents for the treatment (or prevention) of various cardiomyopathies.

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Section: Discussionmentioning

confidence: 99%

H2S Donors with Cytoprotective Effects in Models of MI/R Injury and Chemotherapy-Induced Cardiotoxicity

Lukesh

2023

Antioxidants

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“…Several recent evidence has led to the attempt to affect the redox status of the myocardium to restore the necessary biochemical balance. For example, it has been shown that H2S therapy enhances phosphorylation and nuclear localization of nuclear factor erythroid 2-related factor 2 (NRF2), leading to the expression of NRF2-targeted downstream anti-oxidative stress genes, thus protecting cardiac tissue against I/R injury [37]. Moreover, antioxidants, free radical scavengers and traditional Chinese medicine can also protect against myocardial damage in ischemic heart disease [38][39][40][41][42].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of time-dependent phenotypes of myocardial ischemia-reperfusion in mice

Meng,

Yuan,

Zhou

et al. 2023

Aging

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Background: A mouse model of myocardial ischemia-reperfusion (I/R) is widely used to study myocardial ischemia-reperfusion injury (I/RI). However, few studies focus on the direct comparison of the extent of pathological events resulting from variant durations of ischemia and reperfusion process. Methods: A mouse model of I/RI was established by ligation and perfusion of the left anterior descending coronary artery (LAD), and the dynamic changes were recorded by electrocardiogram at different stages of I/R. Subsequently, reperfusion duration was used as a variable to directly compare the phenotypes of different myocardial injury degrees induced by 3 h, 6 h and 24 h reperfusion from myocardial infarct size, myocardial apoptosis, myocardial enzyme, and inflammatory cytokine levels. Results: All mice subjected to myocardial I/R surgery showed obvious myocardial infarction, extensive myocardial apoptosis, dynamic changes in serum myocardial enzyme and inflammatory cytokines, at least for the first 24 h of reperfusion. The infarct size and apoptosis rates gradually increased with the extension of reperfusion time. The peaks of serum myocardial enzyme and inflammatory cytokines occurred at 6 h and 3 h of reperfusion, respectively. We also established I/R mice models with 30 and 60 mins of ischemia. After 21 days of remodeling, longer periods of ischemia increased the degree of fibrosis and reduced cardiac function. Conclusions: In summary, we conclude that reperfusion durations of 3 h, 6 h, and 24 h induces different injury phenotypes in ischemia-reperfusion mouse model. At the same time, the ischemia duration before reperfusion also affects the degree of cardiac remodeling.

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“…The Nrf2/ARE axis act as key signaling molecules in preventing oxidative damage of cardiac cell [ 153 ] and protects the heart against cardiac dysfunction and maladaptive remodeling [ 154 , 155 ]. Previous studies demonstrated that Nrf2 signaling is involved in the onset and progression of numerous heart disorders, including MI, myocarditis and atrial fibrillation [ 156 , 157 ]. Nrf2/HO-1 activation upregulates the transcription of several endogenous antioxidants and protects cardiomyocytes from damage caused by oxygen radicals [ 158 ].…”

Section: Cardiac Diseasesmentioning

confidence: 99%

Nrf2 activation: a key mechanism in stem cell exosomes-mediated therapies

Vahidinia,

Azami Tameh,

Barati

et al. 2024

Cell Mol Biol Lett

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Exosomes are nano-sized membrane extracellular vesicles which can be released from various types of cells. Exosomes originating from inflammatory or injured cells can have detrimental effects on recipient cells, while exosomes derived from stem cells not only facilitate the repair and regeneration of damaged tissues but also inhibit inflammation and provide protective effects against various diseases, suggesting they may serve as an alternative strategy of stem cells transplantation. Exosomes have a fundamental role in communication between cells, through the transfer of proteins, bioactive lipids and nucleic acids (like miRNAs and mRNAs) between cells. This transfer significantly impacts both the physiological and pathological functions of recipient cells. Nuclear factor erythroid 2–related factor 2 (Nrf2), a transcription factor, is able to mitigate damage caused by oxidative stress and inflammation through various signaling pathways. The positive effects resulting from the activation of the Nrf2 signaling pathway in different disorders have been documented in various types of literature. Studies have confirmed that exosomes derived from stem cells could act as Nrf2 effective agonists. However, limited studies have explored the Nrf2 role in the therapeutic effects of stem cell-derived exosomes. This review provides a comprehensive overview of the existing knowledge concerning the role of Nrf2 signaling pathways in the impact exerted by stem cell exosomes in some common diseases. Graphical Abstract

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The cardioprotective effects of hydrogen sulfide by targeting endoplasmic reticulum stress and the Nrf2 signaling pathway: A review

Cited by 17 publications

References 106 publications

H2S Donors with Cytoprotective Effects in Models of MI/R Injury and Chemotherapy-Induced Cardiotoxicity

H2S Donors with Cytoprotective Effects in Models of MI/R Injury and Chemotherapy-Induced Cardiotoxicity

Evaluation of time-dependent phenotypes of myocardial ischemia-reperfusion in mice

Nrf2 activation: a key mechanism in stem cell exosomes-mediated therapies

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