Advancements in omics technologies: Molecular mechanisms of acute lung injury and acute respiratory distress syndrome (Review).

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is an inflammatory response arising from lung and systemic injury with diverse causes and associated with high rates of morbidity and mortality. To date, no fully effective pharmacological therapies have been established and the relevant underlying mechanisms warrant elucidation, which may be facilitated by multi‑omics technology. The present review summarizes the application of multi‑omics technology in identifying novel diagnostic markers and therapeutic strategies of ALI/ARDS as well as its pathogenesis.

Role of gut microbes in acute lung injury/acute respiratory distress syndrome.

Acute lung injury (ALI) is an acute, diffuse inflammatory lung condition triggered by factors of severe infections, trauma, shock, burns, ischemia-reperfusion, and mechanical ventilation. It is primarily characterized by refractory hypoxemia and respiratory distress. The more severe form, acute respiratory distress syndrome (ARDS), can progress to multi-organ failure and has a high mortality rate.

Metabolic disorders, inter-organ crosstalk, and inflammation in the progression of metabolic dysfunction-associated steatotic liver disease.

Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a global health concern, affecting over 30 % of adults. It is a principal driver in the development of cirrhosis and hepatocellular carcinoma. The complex pathogenesis of MASLD involves an excessive accumulation of lipids, subsequently disrupting lipid metabolism and prompting inflammation within the liver.

miR1432 negatively regulates cold tolerance by targeting OsACAs.

miRNAs function as negative regulators that significantly influence plant growth and stress responses. Within rice and other monocotyledonous plants, miR1432 plays a conserved role in seed development and disease resistance. However, its involvement in the response to abiotic stresses remains unclear.

Endothelial cell dynamics in sepsis-induced acute lung injury and acute respiratory distress syndrome: pathogenesis and therapeutic implications.

Sepsis, a prevalent critical condition in clinics, continues to be the leading cause of death from infections and a global healthcare issue. Among the organs susceptible to the harmful effects of sepsis, the lungs are notably the most frequently affected. Consequently, patients with sepsis are predisposed to developing acute lung injury (ALI), and in severe cases, acute respiratory distress syndrome (ARDS).

Inhibition of PPARγ by BZ26, a GW9662 derivate, attenuated obesity-related breast cancer progression by inhibiting the reprogramming of mature adipocytes into to cancer associate adipocyte-like cells.

Obesity has been associated with the development of 13 different types of cancers, including breast cancer. Evidence has indicated that cancer-associated adipocytes promote the proliferation, invasion, and metastasis of cancer. However, the mechanisms that link CAAs to the progression of obesity-related cancer are still unknown.

The great potential of flavonoids as candidate drugs for NAFLD.

Non-alcoholic fatty liver disease (NAFLD) has a global prevalence of approximately 25 % and is associated with high morbidity and high mortality. NAFLD is a leading cause of cirrhosis and hepatocellular carcinoma. Its pathophysiology is complex and still poorly understood, and there are no drugs used in the clinic to specifically treat NAFLD.

An overview of ferroptosis in non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) is a public health problem associated with high mortality and high morbidity rates worldwide. Presently, its complex pathophysiology is still unclear, and there is no specific drug to reverse NAFLD. Ferroptosis is an iron-dependent and non-apoptotic form of cell death characterized by the iron-induced accumulation of lipid reactive oxygen species (ROS), which damage nucleic acids, proteins, and lipids; generate intracellular oxidative stress; and ultimately cause cell death.

TLR7 Mediates Acute Respiratory Distress Syndrome in Sepsis by Sensing Extracellular miR-146a.

TLR7 (Toll-like receptor 7), the sensor for single-stranded RNA, contributes to systemic inflammation and mortality in murine polymicrobial sepsis. Recent studies show that extracellular miR-146a-5p serves as a TLR7 ligand and plays an important role in regulating host innate immunity. However, the role of miR-146a-5p and TLR7 signaling in pulmonary inflammation, endothelial activation, and sepsis-associated acute respiratory distress syndrome remains unclear.

The links between gut microbiota and obesity and obesity related diseases.

The obesity epidemic has become a global public health crisis in recent years and is continuing to worsen at an alarming rate. However, the pathophysiological mechanisms involved in the development of obesity and obesity-related diseases are still being unraveled. In the past ten years, the gut microbiota has been identified as a crucial player affecting the onset and progression of obesity and obesity-related diseases, especially with respect to changes in its composition and metabolites during obesity progression.

Isolating High Antimicrobial Ability Lignin From Bamboo Kraft Lignin by Organosolv Fractionation.

Lignin from different biomasses possess biological antioxidation and antimicrobial activities, which depend on the number of functional groups and the molecular weight of lignin. In this work, organosolv fractionation was carried out to prepare the lignin fraction with a suitable structure to tailor excellent biological activities. Gel permeation chromatography (GPC) analysis showed that decreased molecular weight lignin fractions were obtained by sequentially organosolv fractionation with anhydrous acetone, 50% acetone and 37.

Autophagy Plays a Protective Role in Sodium Hydrosulfide-Induced Acute Lung Injury by Attenuating Oxidative Stress and Inflammation in Rats.

Sodium hydrosulfide (NaHS), as an exogenous hydrogen sulfide (HS) donor, has been used in various pathological models. NaHS is usually considered to be primarily protective, however, the toxic effect of NaHS has not been well elucidated. The aim of this study was to investigate whether NaHS (1 mg/kg) can induce acute lung injury (ALI is a disease process characterized by diffuse inflammation of the lung parenchyma) and define the mechanism by which NaHS-induced ALI involves autophagy, oxidative stress, and inflammatory response.

A novel chrysin thiazole derivative polarizes macrophages to an M1 phenotype via targeting TLR4.

Tumor-associated macrophages (TAMs) are an important cause of tumorigenesis and tumor development. M2 macrophages can promote tumor growth while M1 macrophages kill tumor cells, therefore, polarizing macrophages to achieve a functional M1 phenotype could effectively play its anti-tumor role. In the current study, we synthesized a novel chrysin derivative which is termed as ChR-TD.

5-Fluorouracil Enhances the Antitumor Activity of the Glutaminase Inhibitor CB-839 against -Mutant Colorectal Cancers.

encodes the p110α catalytic subunit of PI3K and is frequently mutated in human cancers, including ∼30% of colorectal cancer. Oncogenic mutations in render colorectal cancers more dependent on glutamine. Here we report that the glutaminase inhibitor CB-839 preferentially inhibits xenograft growth of -mutant, but not wild-type (WT), colorectal cancers.

Lycopene ameliorates chronic stress-induced hippocampal injury and subsequent learning and memory dysfunction through inhibiting ROS/JNK signaling pathway in rats.

The natural carotenoid lycopene (LYC) has strong antioxidant and neuroprotective capacities. This study investigated the effects and mechanisms of LYC on chronic stress-induced hippocampal lesions and learning and memory dysfunction. Rats were administered LYC and/or chronic restraint stress (CRS) for 21 days.

P-STAT3 Inhibition Activates Endoplasmic Reticulum Stress-Induced Splenocyte Apoptosis in Chronic Stress.

Chronic stress leads to immunosuppression and induces splenocyte apoptosis. STAT3 is a transcription factor that regulates immunity and apoptosis; however, it is unclear whether the increased expression of phosphorylated STAT3 (p-STAT3) observed in chronic stress is related to splenocyte apoptosis. To explore the relationship between splenocyte apoptosis and STAT3 in chronic stress, we treated rats undergoing a 21-day chronic restraint stress program with the STAT3 inhibitor S3I-201.

Dexmedetomidine Enhances Autophagy α2-AR/AMPK/mTOR Pathway to Inhibit the Activation of NLRP3 Inflammasome and Subsequently Alleviates Lipopolysaccharide-Induced Acute Kidney Injury.

Background: Acute kidney injury (AKI) is a severe complication of sepsis; however, no effective drugs have been found. Activation of the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome is a major pathogenic mechanism of AKI induced by lipopolysaccharide (LPS). Autophagy, a process of intracellular degradation related to renal homeostasis, effectively restricts inflammatory responses.

OsJAZ13 Negatively Regulates Jasmonate Signaling and Activates Hypersensitive Cell Death Response in Rice.

Jasmonate ZIM-domain (JAZ) proteins belong to the subgroup of TIFY family and act as key regulators of jasmonate (JA) responses in plants. To date, only a few JAZ proteins have been characterized in rice. Here, we report the identification and function of rice gene.

Dexmedetomidine Protects Against Lipopolysaccharide-Induced Acute Kidney Injury by Enhancing Autophagy Through Inhibition of the PI3K/AKT/mTOR Pathway.

Background: Acute kidney injury (AKI) is often secondary to sepsis. Previous studies suggest that damaged mitochondria and the inhibition of autophagy results in AKI during sepsis, but dexmedetomidine (DEX) alleviates lipopolysaccharide (LPS)-induced AKI. However, it is uncertain whether the renoprotection of DEX is related to autophagy or the clearance of damaged mitochondria in sepsis-induced AKI.

Role of c-Myc/chloride intracellular channel 4 pathway in lipopolysaccharide-induced neurodegenerative diseases.

LPS-induced neuronal apoptosis leads to neurodegenerative diseases (NDs). However, the mechanisms underlying NDs pathogenesis remains unclear. The apoptotic response to activation of the c-Myc/chloride intracellular channel (CLIC4) pathway is directed through a mitochondrial pathway.

Toxic effects of hydrogen sulfide donor NaHS induced liver apoptosis is regulated by complex IV subunits and reactive oxygen species generation in rats.

In recent years, the protective effect of hydrogensulfide donor sodium hydrosulfide(NaHS) on multiple organs has been widely reported. The study aimed to explorethe effect of commonly used concentration of NaHS on theliver and its potential damage mechanism. Rats divided into 4 groups: control, NaHS I (1 mg/kg), II (3 mg/kg) and III(5 mg/kg) groups, and each group is divided into four-timepoints (2, 6, 12, and 24 hours).

Glucocorticoid-Driven NLRP3 Inflammasome Activation in Hippocampal Microglia Mediates Chronic Stress-Induced Depressive-Like Behaviors.

Chronic stress is a key risk factor for depression, and microglia have been implicated in the pathogenesis of the disease. Recent studies show that the Nod-like receptor protein 3 (NLRP3) inflammasome is expressed in microglia and may play a crucial role in depression. However, the mechanism of NLRP3 inflammasome activation in hippocampal microglia and its role in depressive-like behaviors remain poorly understood.

Dexmedetomidine ameliorates LPS induced acute lung injury via GSK-3β/STAT3-NF-κB signaling pathway in rats.

Acute lung injury (ALI) is a serious complication of sepsis and an important cause of death in intensive care. Studies have shown that DEX can inhibit inflammation. However, the anti-inflammatory effect and protective mechanism of DEX in lipopolysaccharide (LPS) induced ALI are still unclear.

Dexmedetomidine alleviates lipopolysaccharide-induced acute kidney injury by inhibiting the NLRP3 inflammasome activation via regulating the TLR4/NOX4/NF-κB pathway.

Dexmedetomidine (DEX) prevents kidney damage caused by sepsis, but the mechanism of this effect remains unclear. In this study, the protective molecular mechanism of DEX in lipopolysaccharide (LPS)-induced acute kidney injury was investigated and its potential pharmacological targets from the perspective of inhibiting oxidative stress damage and the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome activation. Intraperitoneal injection of DEX (30 μg/kg) significantly improved LPS (10 mg/kg) induced renal pathological damage and renal dysfunction.