Protective effect of H<sub>2</sub>S on LPS‑induced AKI by promoting autophagy

T, Li; Zhao, Jie; Miao, Shuying; Chen, Yiyang; Xu, Yunfei; Liu, Ying

doi:10.3892/mmr.2022.12612

Cited by 9 publications

(7 citation statements)

References 52 publications

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“…Zheng et al (22) also confirmed that autophagy was enhanced in SI-AKI. They next found that downregulation of ataxia-telangiectasia mutated (ATM) significantly suppressed autophagy and inflammatory response in (35). LPS can increase the production of intracellular ROS via Toll-like Receptor 4 (TLR4), which can lead to mitochondrial damage and activate platelets.…”

Section: Other Potential Mechanismsmentioning

confidence: 99%

“…The following information was noted, including the first author of the included studies, year of publication, experimental model or participant, methods for establishing sepsis-induced AKI, the status of autophagy, associated genes or pathways in the action of autophagy, and the main findings of the relevant studies. Finally, there were 41 experimental and clinical studies (7, 14-33) (34)(35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51)(52)(53) included in the review. The selection process for screening the relevant studies shown in Supplementary Figure 1.…”

Section: A Search Of the Literaturementioning

confidence: 99%

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Epigenetic dysregulation of autophagy in sepsis-induced acute kidney injury: the underlying mechanisms for renoprotection

et al. 2023

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Sepsis-induced acute kidney injury (SI-AKI), a common critically ill, represents one of the leading causes of global death. Emerging evidence reveals autophagy as a pivotal modulator of SI-AKI. Autophagy affects the cellular processes of renal lesions, including cell death, inflammation, and immune responses. Herein, we conducted a systematic and comprehensive review on the topic of the proposed roles of autophagy in SI-AKI. Forty-one relevant studies were finally included and further summarized and analyzed. This review revealed that a majority of included studies (24/41, 58.5%) showed an elevation of the autophagy level during SI-AKI, while 22% and 19.5% of the included studies reported an inhibition and an elevation at the early stage but a declination of renal autophagy in SI-AKI, respectively. Multiple intracellular signaling molecules and pathways targeting autophagy (e.g. mTOR, non-coding RNA, Sirtuins family, mitophagy, AMPK, ROS, NF-Kb, and Parkin) involved in the process of SI-AKI, exerting multiple biological effects on the kidney. Multiple treatment modalities (e.g. small molecule inhibitors, temsirolimus, rapamycin, polydatin, ascorbate, recombinant human erythropoietin, stem cells, Procyanidin B2, and dexmedetomidine) have been found to improve renal function, which may be attributed to the elevation of the autophagy level in SI-AKI. Though the exact roles of autophagy in SI-AKI have not been well elucidated, it may be implicated in preventing SI-AKI through various molecular pathways. Targeting the autophagy-associated proteins and pathways may hint towards a new prospective in the treatment of critically ill patients with SI-AKI, but more preclinical studies are still warranted to validate this hypothesis.

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Section: Other Potential Mechanismsmentioning

confidence: 99%

Section: A Search Of the Literaturementioning

confidence: 99%

Epigenetic dysregulation of autophagy in sepsis-induced acute kidney injury: the underlying mechanisms for renoprotection

et al. 2023

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“…NaHS has been reported to enhance LPS-induced SIC via regulation of signaling pathways, such as the toll-like receptor 4 pathway, and endoplasmic reticulum stress ( 21 ). Although NaHS has been widely investigated in the prevention and treatment of sepsis ( 22 , 23 ), its regulatory mechanisms and involvement in ferroptosis regulation in SIC require further elucidation. In the present study, an in vitro model of LPS-induced H9c2 cardiomyocyte injury and an in vivo model of CLP-induced sepsis were employed to determine whether the H 2 S donor NaHS alleviates septic myocardial injury by decreasing oxidative stress and cardiomyocyte ferroptosis.…”

Section: Introductionmentioning

confidence: 99%

H2S regulation of ferroptosis attenuates sepsis‑induced cardiomyopathy

et al. 2022

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Ferroptosis is a non-apoptotic form of cell death mediated by reactive oxygen species (ROS). Iron metabolism disorders play a key role in sepsis-induced cardiomyopathy (SIC). While hydrogen sulfide (H 2 S) inhibits SIC, it is unknown if it does so by controlling ferroptosis. The present study evaluated whether sodium hydrosulfide (NaHS), an H 2 S donor, alleviates SIC by decreasing ferroptosis. Lipopolysaccharide (LPS) was employed to induce an in vitro model of septic myocardial injury in rat H9c2 cardiomyocytes. The myocardial injury model of septic rats was established by cecal ligation and puncture (CLP). Cardiomyocyte injury was evaluated using Cell Counting Kit-8 and myocardial enzyme assay and hematoxylin and eosin (H&E) staining. The cardiac function of rats was assessed using echocardiography and changes in myocardial fibers and mitochondria were evaluated using H&E staining and transmission electron microscopy, respectively. Fe 2+ , glutathione and malondialdehyde levels in cardiomyocytes were detected using assay kits, ROS and mitochondrial membrane potential changes were detected using fluorescent probes and ferroptosis and Beclin 1 (BECN1) signaling pathway-associated protein expression levels were semi-quantified using western blotting. NaHS decreased ferroptosis of H9c2 cells induced by LPS and decreased injury of myocardial cells by improving iron metabolism disorder and oxidative stress levels. Furthermore, in vivo results demonstrated that NaHS attenuated CLP-induced septic myocardial ferroptosis and significantly improved cardiac dysfunction in septic rats compared with the CLP group. NaHS was demonstrated to attenuate sepsis-induced myocardial cell and tissue injury by significantly inhibiting the phosphorylation of BECN1 and significantly increasing expression levels of the ferroptosis regulatory proteins solute carrier family 7 member 11 and glutathione peroxidase 4. The results of the present study suggested that by regulating the BECN1 signaling pathway, NaHS may decrease the incidence of myocardial ferroptosis, thereby improving SIC.

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“…1,2 As an essential gas signal molecule, H 2 S mediates various physiological processes such as nerve signal transmission, angiogenesis, anti-oxidation, anti-apoptotic and anti-inflammatory processes, providing support and protection to cells. 3–5 Besides this, it has been confirmed that abnormal levels of H 2 S have close connection with diseases such as Alzheimer's disease, Huntington's disease, Parkinson's disease, diabetes, liver cirrhosis and ulcerative colitis. 6–9 Ulcerative colitis (UC) is a kind of inflammatory bowel disease, which has become a common intestinal disease in many countries and is also listed as one of the most difficult diseases to treat by the World Health Organization.…”

Section: Introductionmentioning

confidence: 77%

A near-infrared fluorescent probe for detecting hydrogen sulfide with high selectivity in cells and ulcerative colitis in mice

Qin,

Yan,

Wang

et al. 2023

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Protective effect of H₂S on LPS‑induced AKI by promoting autophagy

Cited by 9 publications

References 52 publications

Epigenetic dysregulation of autophagy in sepsis-induced acute kidney injury: the underlying mechanisms for renoprotection

Epigenetic dysregulation of autophagy in sepsis-induced acute kidney injury: the underlying mechanisms for renoprotection

H2S regulation of ferroptosis attenuates sepsis‑induced cardiomyopathy

A near-infrared fluorescent probe for detecting hydrogen sulfide with high selectivity in cells and ulcerative colitis in mice

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Protective effect of H2S on LPS‑induced AKI by promoting autophagy

Cited by 9 publications

References 52 publications

Epigenetic dysregulation of autophagy in sepsis-induced acute kidney injury: the underlying mechanisms for renoprotection

Epigenetic dysregulation of autophagy in sepsis-induced acute kidney injury: the underlying mechanisms for renoprotection

H2S regulation of ferroptosis attenuates sepsis‑induced cardiomyopathy

A near-infrared fluorescent probe for detecting hydrogen sulfide with high selectivity in cells and ulcerative colitis in mice

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Protective effect of H₂S on LPS‑induced AKI by promoting autophagy