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Open AccessJournal ArticleDOI

Exogenous H2S Protects Against Diabetic Cardiomyopathy by Activating Autophagy via the AMPK/mTOR Pathway.

TLDR
The findings demonstrated that H2S decreases oxidative stress and protects against mitochondria injury, activates autophagy, and eventually leads to cardiac protection via the AMPK/mTOR pathway.
Abstract
Background/aim Autophagy plays an important role in cellular homeostasis through the disposal and recycling of cellular components. Hydrogen sulphide (H2S) is the third endogenous gas that has been shown to confer cardiac protective effects. Given the regulation of autophagy in cardioprotection, this study aimed to investigate the protective effects of H2S via autophagy during high glucose treatment. Methods This study investigated the content of H2S in the plasma as well as myocardial, ultrastructural changes in mitochondria and autophagosomes. This study also investigated the apoptotic rate using Hoechst/PI as well as expression of autophagy-associated proteins and mitochondrial apoptotic proteins in H9C2 cells treated with or without GYY4137. Mitochondria of cardiac tissues were isolated and RCR and ADP/O were also detected. AMPK knockdown was performed with siRNA transfection. Results In a STZ-induced diabetic model, NaHS treatment not only increased the expression of p-AMPK in diabetic group but further activated cell autophagy. Following 48h high glucose, autophagosomes and cell viability were reduced. The present results showed that autophagy could be induced by H2S, which was verified by autophagic ultrastructural observation and LC3-I/LC3-II conversion. In addition, the mitochondrial membrane potential (MMP) was significantly decreased. The expressions levels of autophagic-related proteins were significantly elevated. Moreover, H2S activated the AMPK/rapamycin (mTOR) signalling pathway. Conclusions Our findings demonstrated that H2S decreases oxidative stress and protects against mitochondria injury, activates autophagy, and eventually leads to cardiac protection via the AMPK/mTOR pathway.

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Journal ArticleDOI

Morpholine as a privileged structure: A review on the medicinal chemistry and pharmacological activity of morpholine containing bioactive molecules.

TL;DR: The medicinal chemistry/pharmacological activity of morpholine derivatives on various therapeutically related molecular targets are described, attempting to highlight the importance of the morpholine ring in drug design and development as well as to justify its classification as a privileged structure.
Journal ArticleDOI

Long noncoding RNA CA7-4 promotes autophagy and apoptosis via sponging MIR877-3P and MIR5680 in high glucose-induced vascular endothelial cells.

TL;DR: This study identified that a small chemical molecule, 3-benzyl-5-([2-nitrophenoxy] methyl)-dihydrofuran-2(3H)-one (3BDO), synthesized by us, could inhibit VEC autophagy and apoptosis induced by a high concentration of glucose.
Journal ArticleDOI

Hydrogen sulfide and autophagy: A double edged sword.

TL;DR: The H2S metabolism in mammals is summarized and the effects of signaling pathways in H 2S‐mediated autophagy are further discussed.
Journal ArticleDOI

Allopurinol reduces oxidative stress and activates Nrf2/p62 to attenuate diabetic cardiomyopathy in rats.

TL;DR: In vitro, ALP increased Nrf2 and reduced the hyperglycaemia‐induced increases of H9C2 cardiomyocyte hypertrophy, oxidative stress, apoptosis and autophagy, and enhanced cellular viability, while in vivo ALP reverted all the above‐mentioned diabetes‐induced biochemical changes.
References
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Journal ArticleDOI

Methods in Mammalian Autophagy Research

TL;DR: Methods to monitor autophagy and to modulate autophagic activity are discussed, with a primary focus on mammalian macroautophagy.
Journal ArticleDOI

Autophagy and the Integrated Stress Response

TL;DR: Autophagy is a cell biological process that is a central component of the integrated stress response and can be integrated with other cellular stress responses through parallel stimulation of autophagy and other stress responses by specific stress stimuli.
Journal ArticleDOI

How to Interpret LC3 Immunoblotting

TL;DR: This work has shown that it is important to measure the amount of LC3-II delivered to lysosomes by comparing LC2-II levels in the presence and absence ofLysosomal protease inhibitors, and that this amount can be compared between samples.
Book ChapterDOI

The respiratory chain and oxidative phosphorylation.

TL;DR: How the respiratory chain and oxidative phosphorylation works and which substances may disable it are explained.
Journal ArticleDOI

Two’s company, three’s a crowd: can H2S be the third endogenous gaseous transmitter?

TL;DR: It is hypothesized that H2S is the third endogenous signaling gasotransmitter, besides nitric oxide and carbon monoxide, and this positioning will open an exciting field‐H2S physiology‐encompassing realization of the interaction of H1N1 and other gasOTransmitters, sulfurating modification of proteins, and the functional role of H2Sin multiple systems.
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The present results showed that autophagy could be induced by H2S, which was verified by autophagic ultrastructural observation and LC3-I/LC3-II conversion.