Promotion of NLRP3 autophagosome degradation by PV-K nanodevice for protection against macrophage pyroptosis-mediated lung injury.

Acute respiratory distress syndrome (ARDS) has emerged as a significant global health challenge, with no definitive curative treatment available. Recent evidence suggests that pyroptosis of immune cells plays a pivotal role in the pathogenesis of ARDS. Targeting and modulating immune cell pyroptosis in lung tissue may offer a promising strategy to mitigate the harmful inflammation associated with this condition.

Interaction, diagnosis, and treatment of lung microbiota-NLRP3 inflammasome-target organ axis in sepsis.

Sepsis is defined as a life-threatening condition caused by a dysregulated host response to infection, leading to multi-organ dysfunction, and representing a significant global health burden. The progression of sepsis is closely linked to disruptions in lung microbiota, including bacterial translocation, impaired barrier function, and local microenvironmental disturbances. Conversely, the worsening of sepsis exacerbates lung microbiota imbalances, contributing to multi-organ dysfunction.

Genetic analysis of diagnostic and therapeutic potential for ferroptosis in postoperative sepsis.

Background: Ferroptosis is a new form of iron-dependent cell death that is closely associated with sepsis. However, few studies have investigated the diagnostic and therapeutic potential for ferroptosis-related genes (FRGs) among postoperative sepsis.

Methods: The GSE131761 dataset was used to identify differentially expressed FRGs (DE-FRGs).

Long-term trends and comparison of the burden of lower respiratory tract infections in China and globally from 1990 to 2021: an analysis based on the Global Burden of Disease study 2021.

Background: This study aimed to describe the temporal trends in the age and sex burdens of lower respiratory infections (LRIs) in China and globally from 1990 to 2021 and to analyze their epidemiological characteristics to formulate corresponding strategies to control LRIs.

Methods: This study utilized open data from the Global Burden of Disease (GBD) database from 1990 to 2021 to assess the burden of disease based on the prevalence, incidence, mortality, years lost (YLLs), years lived with disability (YLDs), and disability-adjusted life-years (DALYs) of LRIs in China and globally. Moreover, a comprehensive comparative analysis of the epidemiological characteristics of LRIs in China and globally was conducted via the Joinpoint regression model, age-period-cohort model (APC model), and stratified analysis of the study method from multiple dimensions, such as age, sex, and period.

Inhibition of Golgi stress alleviates sepsis-induced cardiomyopathy by reducing inflammation and apoptosis.

Background: Sepsis is often accompanied by multiple organ dysfunction, in which the incidence of cardiac injury is about 60%, and is closely related to high mortality. Recent studies have shown that Golgi stress is involved in liver injury, kidney injury, and lung injury in sepsis. However, whether it is one of the key mechanisms of sepsis-induced cardiomyopathy (SIC) is still unclear.

Molecular hydrogen attenuates sepsis-induced cardiomyopathy in mice by promoting autophagy.

Background: Approximately 40 to 60% of patients with sepsis develop sepsis-induced cardiomyopathy (SIC), which is associated with a substantial increase in mortality. We have found that molecular hydrogen (H) inhalation improved the survival rate and cardiac injury in septic mice. However, the mechanism remains unclear.

THE PROTECTIVE EFFECT OF DEXMEDETOMIDINE ON THE LIVER INJURY IN SEPSIS THROUGH INHIBITION OF NECROPTOSIS.

Background: Sepsis-induced liver injury leads to extensive necroptosis in hepatocytes, which is the main factor of liver dysfunction. This study aims to investigate the protective effect of dexmedetomidine (DEX) on septic liver and to explore whether its molecular mechanism is related to the modulation of necroptosis. Methods: The model of septic liver injury was induced by cecal ligation and puncture (CLP) in rats.

Molecular hydrogen attenuates sepsis-induced cognitive dysfunction through regulation of tau phosphorylation.

Background: Sepsis-associated encephalopathy (SAE) is a cognitive dysfunction caused by sepsis. Hyperphosphorylated tau is considered to play a significant role in the progression of neurodegenerative disease and also contributes to cognitive dysfunction in septic mice. Molecular hydrogen (H) plays an antioxidant and anti-inflammatory role, and plays a protective role in septic mice.

Clemastine Fumarate Attenuates Myocardial Ischemia Reperfusion Injury Through Inhibition of Mast Cell Degranulation.

Mast cell (MC) activation is associated with myocardial ischemia reperfusion injury (MIRI). Suppression of MC degranulation might be a target of anti-MIRI. This study aimed to determine whether clemastine fumarate (CLE) could attenuate MIRI by inhibiting MC degranulation.

Dexmedetomidine attenuates myocardial ischemia-reperfusion injury in vitro by inhibiting NLRP3 Inflammasome activation.

Background: Myocardial ischemia-reperfusion injury (MIRI) is the most common cause of death worldwide. The NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome plays an important role in the inflammatory response to MIRI. Dexmedetomidine (DEX), a specific agonist of α2-adrenergic receptor, is commonly used for sedation and analgesia in anesthesia and critically ill patients.