Polydatin Improves Sepsis-Associated Encephalopathy by Activating Sirt1 and Reducing p38 Phosphorylation

Huang, Liwei; Chen, Jiawei; Li, Xiaojie; Huang, Mingxin; Liu, Jilou; Qin, N; Zeng, Zhenhua; Wang, Xingmin; Li, Fen; Yang, Hong

doi:10.1016/j.jss.2022.03.008

Cited by 5 publications

(2 citation statements)

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“…193 On the other hand, activation of the cytosolic complex promotes cell survival and proinflammatory signaling through NF-κB and MAPK activation. 194,195 However, the mechanisms that determine whether a cell undergoes apoptosis, necroptosis, or cell survival are still not fully understood. Genetic studies have shown that deficiencies in FADD or Caspase-8 can result in RIPK3-mediated necroptosis, leading to embryonic lethality and inflammation.…”

Section: Necroptosismentioning

confidence: 99%

“…Furthermore, the recruitment of RIPK1 to FAS without an inhibitor of apoptosis leads to the assembly of necrosomes and necroptosis 193 . On the other hand, activation of the cytosolic complex promotes cell survival and proinflammatory signaling through NF‐κB and MAPK activation 194,195 . However, the mechanisms that determine whether a cell undergoes apoptosis, necroptosis, or cell survival are still not fully understood.…”

Section: Regulatory Mechanisms Involved In Sepsismentioning

confidence: 99%

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The pathogenesis and potential therapeutic targets in sepsis

Zhang,

Jiang,

et al. 2023

MedComm

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Sepsis is defined as “a life‐threatening organ dysfunction caused by dysregulated host systemic inflammatory and immune response to infection.” At present, sepsis continues to pose a grave healthcare concern worldwide. Despite the use of supportive measures in treating traditional sepsis, such as intravenous fluids, vasoactive substances, and oxygen plus antibiotics to eradicate harmful pathogens, there is an ongoing increase in both the morbidity and mortality associated with sepsis during clinical interventions. Therefore, it is urgent to design specific pharmacologic agents for the treatment of sepsis and convert them into a novel targeted treatment strategy. Herein, we provide an overview of the molecular mechanisms that may be involved in sepsis, such as the inflammatory response, immune dysfunction, complement deactivation, mitochondrial damage, and endoplasmic reticulum stress. Additionally, we highlight important targets involved in sepsis‐related regulatory mechanisms, including GSDMD, HMGB1, STING, and SQSTM1, among others. We summarize the latest advancements in potential therapeutic drugs that specifically target these signaling pathways and paramount targets, covering both preclinical studies and clinical trials. In addition, this review provides a detailed description of the crosstalk and function between signaling pathways and vital targets, which provides more opportunities for the clinical development of new treatments for sepsis.

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Section: Necroptosismentioning

confidence: 99%

Section: Regulatory Mechanisms Involved In Sepsismentioning

confidence: 99%