Correction to ‘
            <i>ALOX5, LPA, MMP9</i>
            and
            <i>TPO</i>
            gene polymorphisms increase atherothrombosis susceptibility in middle-aged Mexicans’

Camacho-Mejorado, Rafael; Gómez, Rocío; Torres‐Sánchez, Luisa; Hernández-Tobías, Esther Alhelí; Noris, Gino; Santana, Carla; Magaña, Jonathan J; Orozco, Lorena; Peña-Dı́az, Aurora de la; Arenas-Sordo, María de la Luz; Meraz-Ríos, Marco Antonio; Majluf‐Cruz, Abraham

doi:10.1098/rsos.200167

Cited by 1 publication

(2 citation statements)

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“…274,310,311 HMGB1 also binds to cellular receptors for RAGE that enter the lysosomes of macrophages and ECs and trigger activation of the transcription factors NF-κB and MAPK. 312 In addition, HMGB1 destabilizes lysosomal membranes and promotes LPS release into the cytoplasm, leading to pyroptosis, and thus promoting lethal coagulation. [313][314][315] These results establish a pathway dependent on DAMP for the transportation of LPS into the cytoplasm, triggering the activation of CASP11 and coagulation.…”

Section: Hmgb1: Crucial Intermediators Between Inflammation and Coagu...mentioning

confidence: 99%

“…As a late‐phase alarmin in sepsis, HMGB1 interacts with RAGE to deliver cytosolic LPS, consequently activating the NLRP3 inflammasome in murine macrophages and lung ECs, leading to caspase‐11‐dependent pyroptosis 274,310,311 . HMGB1 also binds to cellular receptors for RAGE that enter the lysosomes of macrophages and ECs and trigger activation of the transcription factors NF‐κB and MAPK 312 . In addition, HMGB1 destabilizes lysosomal membranes and promotes LPS release into the cytoplasm, leading to pyroptosis, and thus promoting lethal coagulation 313–315 .…”

Section: Potential Therapeutic Targets: Signaling Modulatorsmentioning

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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