Hydrogen sulfide attenuates ferroptosis and stimulates autophagy by blocking mTOR signaling in sepsis-induced acute lung injury

Li, Jianhua; Li, Mengyu; Li, Ling; Ma, Jiamin; Yao, Chengye; Yao, Shanglong

doi:10.1016/j.molimm.2021.12.003

Cited by 79 publications

(51 citation statements)

References 58 publications

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“…H 2 S inhibits ferroptosis by suppressing ALOX12 acetylation and controlling the stability of the xCT (the functional submit of the Xc system), according to Wang and Chen et al [ 216 , 222 ]. Therapy with the H 2 S donor GYY4137 reduces ferroptosis, which helps to reduce acute lung damage [ 223 ]. In hepatocellular carcinoma, inhibiting H 2 S generation with the CBS inhibitor CH004 supplement worsens ferroptosis [ 224 ].…”

Section: H 2 S and Ferroptosismentioning

confidence: 99%

Hydrogen Sulfide Biology and Its Role in Cancer

et al. 2022

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Hydrogen sulfide (H2S) is an endogenous biologically active gas produced in mammalian tissues. It plays a very critical role in many pathophysiological processes in the body. It can be endogenously produced through many enzymes analogous to the cysteine family, while the exogenous source may involve inorganic sulfide salts. H2S has recently been well investigated with regard to the onset of various carcinogenic diseases such as lung, breast, ovaries, colon cancer, and neurodegenerative disorders. H2S is considered an oncogenic gas, and a potential therapeutic target for treating and diagnosing cancers, due to its role in mediating the development of tumorigenesis. Here in this review, an in-detail up-to-date explanation of the potential role of H2S in different malignancies has been reported. The study summarizes the synthesis of H2S, its roles, signaling routes, expressions, and H2S release in various malignancies. Considering the critical importance of this active biological molecule, we believe this review in this esteemed journal will highlight the oncogenic role of H2S in the scientific community.

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Section: H 2 S and Ferroptosismentioning

confidence: 99%

Hydrogen Sulfide Biology and Its Role in Cancer

et al. 2022

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“…Moreover, the AMPK/mTOR pathway is a switch between anabolic and catabolic processes in the cell. Ferroptosis in sepsis-induced acute lung damage has been shown that it can be attenuated by blocking mTOR signaling and autophagy [ 67 ]. Clara secretory cell protein (CC16), a natural anti-inflammatory factor in the lung, inhibits lung injury by activating the PI3K/AKT/mTOR/ERK1/2 pathway to promote A549 cell proliferation and inhibit LPS-induced apoptosis [ 68 ].…”

Section: Signaling Pathways Related To Ali/ardsmentioning

confidence: 99%

Classic Signaling Pathways in Alveolar Injury and Repair Involved in Sepsis-Induced ALI/ARDS: New Research Progress and Prospect

Chen

et al. 2022

Disease Markers

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Sepsis is a common critical clinical disease with high mortality that can cause approximately 10 million deaths worldwide each year. Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) is a common clinical complication of sepsis, which occurs primarily as diffuse alveolar injury, hypoxemia, and respiratory distress. The mortality rate of ALI/ARDS is as high as 30%-40%, which greatly endangers human health. Due to the unclear pathogenesis of ALI/ARDS, its treatment is still a worldwide problem. At present, clinical treatment mainly relies on lung-protective ventilation, prone position ventilation, and fluid management. However, there is a lack of effective and specific treatment measures. In recent years, domestic and foreign scholars have committed to basic research on ALI/ARDS, trying to further clarify its pathogenesis and find new targets and methods for the treatment of ALI/ARDS. In this review, we summarize the signaling pathways related to alveolar injury and repair in sepsis-induced ALI/ARDS and their latest research progress. They include the NF-κB, JAK2/STAT3, mitogen-activated protein kinase (MAPK), mTOR, and Notch signaling pathways. Understanding the molecular mechanisms of these signaling pathways in sepsis-induced ALI/ARDS may provide new targets and ideas for the clinical treatment of this disease.

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“…In addition, it is reported that the preservation of mitochondrial function by NaHS treatment resulted in the improvement of diaphragm weakness and the decline of mortality rate in CLP-induced sepsis rats [ 153 ]. More recently, two studies have shown that the pretreatment of GYY4137 (25 mg/kg and 50 mg/kg intraperitoneal injection), a novel slow-releasing H 2 S donor, protected against acute lung injury caused by CLP-induced sepsis in mice [ 154 , 155 ]. A similar salutary effect of H 2 S was also reported in urinary-derived sepsis, pseudomonas aeruginosa sepsis and pneumococcal pneumosepsis, together with LPS-induced endotoxemia [ 21 , 156 , 157 , 158 , 159 ].…”

Section: Gaseous Mediators In Sepsis/septic Shockmentioning

confidence: 99%

“…Accumulating evidence has revealed the complicated actions played by H 2 S in sepsis, leading to the increasing attention being paid to develop therapeutic approaches targeting H 2 S for sepsis. Although several preclinical animal studies have shown the protective role of using PAG in sepsis [ 136 , 141 ], many other investigations have also indicated that the administration of inhaled H 2 S or H 2 S donors, either fast-releasing donors or slow-releasing donors, such as NaHS and GYY4137, is beneficial to sepsis and endotoxemia, resulting in uncertainties in the possible role of H 2 S-based treatment for sepsis [ 20 , 152 , 153 , 154 , 155 ]. Given the promise of the countermeasures targeting gaseous mediators in sepsis therapy, the establishment of an optimal therapeutic protocol, including the dose and delivery, for gaseous-mediator-based therapy for sepsis will be meaningful and another step forward.…”

Section: Gaseous-mediator-based Therapeutic Strategy For Sepsis/septi...mentioning

confidence: 99%

Gases in Sepsis: Novel Mediators and Therapeutic Targets

Zhu

Chambers

Zeng

et al. 2022

IJMS

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Sepsis, a potentially lethal condition resulting from failure to control the initial infection, is associated with a dysregulated host defense response to pathogens and their toxins. Sepsis remains a leading cause of morbidity, mortality and disability worldwide. The pathophysiology of sepsis is very complicated and is not yet fully understood. Worse still, the development of effective therapeutic agents is still an unmet need and a great challenge. Gases, including nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H2S), are small-molecule biological mediators that are endogenously produced, mainly by enzyme-catalyzed reactions. Accumulating evidence suggests that these gaseous mediators are widely involved in the pathophysiology of sepsis. Many sepsis-associated alterations, such as the elimination of invasive pathogens, the resolution of disorganized inflammation and the preservation of the function of multiple organs and systems, are shaped by them. Increasing attention has been paid to developing therapeutic approaches targeting these molecules for sepsis/septic shock, taking advantage of the multiple actions played by NO, CO and H2S. Several preliminary studies have identified promising therapeutic strategies for gaseous-mediator-based treatments for sepsis. In this review article, we summarize the state-of-the-art knowledge on the pathophysiology of sepsis; the metabolism and physiological function of NO, CO and H2S; the crosstalk among these gaseous mediators; and their crucial effects on the development and progression of sepsis. In addition, we also briefly discuss the prospect of developing therapeutic interventions targeting these gaseous mediators for sepsis.

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Hydrogen sulfide attenuates ferroptosis and stimulates autophagy by blocking mTOR signaling in sepsis-induced acute lung injury

Cited by 79 publications

References 58 publications

Hydrogen Sulfide Biology and Its Role in Cancer

Hydrogen Sulfide Biology and Its Role in Cancer

Classic Signaling Pathways in Alveolar Injury and Repair Involved in Sepsis-Induced ALI/ARDS: New Research Progress and Prospect

Gases in Sepsis: Novel Mediators and Therapeutic Targets

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