The emerging role of adaptor proteins in regulating innate immunity of sepsis.

Sepsis is a life-threatening syndrome caused by a dysregulated immune response. A large number of adaptor proteins have been found to play a pivotal role in sepsis via protein-protein interactions, thus participating in inflammatory cascades, leading to the generation of numerous inflammatory cytokines, as well as oxidative stress and regulated cell death. Although available strategies for the diagnosis and management of sepsis have improved, effective and specific treatments are lacking.

Identification of 18β-glycyrrhetinic acid as an AGT inhibitor against LPS-induced myocardial dysfunction via high throughput screening.

Sepsis induced myocardial dysfunction (SIMD) is a serious complication of sepsis. There is increasing evidence that the renin-angiotensin system (RAS) is activated in SIMD. Angiotensinogen (AGT) is a precursor of the RAS, and the inhibition of AGT may have significant cardiovascular benefits.

The Emerging Role of Ferroptosis in Cardiovascular Diseases.

Ferroptosis is one type of programmed cell death discovered in recent years, which is characterized by iron-dependent lipid peroxidation and participating in iron, lipid and antioxidant metabolism. Ferroptosis is different from the traditional cell death types such as apoptosis, necroptosis and autophagy in morphology, biochemistry and genetics. Cardiovascular diseases are considered as an important cause of death from non-communicable diseases in the global population and poses a serious threat to human health.

Loss of Hepatic Angiotensinogen Attenuates Sepsis-Induced Myocardial Dysfunction.

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Silent existence of eosinopenia in sepsis: a systematic review and meta-analysis.

Background: Sepsis is a life-threatening and time-critical medical emergency; therefore, the early diagnosis of sepsis is essential to timely treatment and favorable outcomes for patients susceptible to sepsis. Eosinopenia has been identified as a potential biomarker of sepsis in the past decade. However, its clinical application progress is slow and its recognition is low.

Therapeutic approaches targeting renin-angiotensin system in sepsis and its complications.

Sepsis, caused by the inappropriate host response to infection, is characterized by excessive inflammatory response and organ dysfunction, thus becomes a critical clinical problem. Commonly, sepsis may progress to septic shock and severe complications, including acute kidney injury (AKI), acute respiratory distress syndrome (ARDS), sepsis-induced myocardial dysfunction (SIMD), liver dysfunction, cerebral dysfunction, and skeletal muscle atrophy, which predominantly contribute to high mortality. Additionally, the global pandemic of coronavirus disease 2019 (COVID-19) raised the concern of development of effectve therapeutic strategies for viral sepsis.

Induction of thoracic aortic dissection: a mini-review of β-aminopropionitrile-related mouse models.

Thoracic aortic dissection (TAD) is one of the most lethal aortic diseases due to its acute onset, rapid progress, and high rate of aortic rupture. The pathogenesis of TAD is not completely understood. In this mini-review, we introduce three emerging experimental mouse TAD models using β-aminopropionitrile (BAPN) alone, BAPN for a prolonged duration (four weeks) and then with added infusion of angiotensin II (AngII), or co-administration of BAPN and AngII chronically.

The emerging role of angiotensinogen in cardiovascular diseases.

Angiotensinogen (AGT) is the unique precursor of all angiotensin peptides. Many of the basic understandings of AGT in cardiovascular diseases have come from research efforts to define its effects on blood pressure regulation. The development of novel techniques targeting AGT manipulation such as genetic animal models, adeno-associated viral approaches, and antisense oligonucleotides made it possible to deeply investigate the relationship between AGT and cardiovascular diseases.

Sirt3 is a novel target to treat sepsis induced myocardial dysfunction by acetylated modulation of critical enzymes within cardiac tricarboxylic acid cycle.

Sepsis induced myocardial dysfunction (SIMD) results in high morbidity and mortality. However, the effective therapeutic strategies for SIMD treatment remain limited. Sirt3 is the main mitochondrial Sirtuin member and is a key modulator of mitochondrial metabolism and function.

Angiotensinogen in hepatocytes contributes to Western diet-induced liver steatosis.

Nonalcoholic fatty liver disease (NAFLD) is considered as a liver manifestation of metabolic disorders. Previous studies indicate that the renin-angiotensin system (RAS) plays a complex role in NAFLD. As the only precursor of the RAS, decreased angiotensinogen (AGT) profoundly impacts RAS bioactivity.

Interleukin 33 in tumor microenvironment is crucial for the accumulation and function of myeloid-derived suppressor cells.

Tumor-induced, myeloid-derived suppressor cells (MDSCs)-mediated immune dysfunction is an important mechanism that leads to tumor immune escape and the inefficacy of cancer immunotherapy. Importantly, tumor-infiltrating MDSCs have much stronger ability compared to MDSCs in the periphery. However, the mechanisms that tumor microenvironment induces the accumulation and function of MDSCs are poorly understood.