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Sepsis-induced organ failure is a major health problem, characterised by massive inflammatory and oxidative stress responses. Endothelin-1 (ET-1) is one of the peptides expressed during septicemia with proapoptotic, proinflammatory, and oxidant effects. ET-1 plays a role in heart and kidney injuries in sepsis. Accordingly, the current study was conducted to investigate, on a mechanistic basis, whether inhibition of ET-1 signalling either by blocking its receptors or inhibiting its formation attenuates sepsis-induced acute cardiorenal injuries. To analyse the role of ET-1 in sepsis, we used a cecal ligation and puncture (CLP) model of sepsis. The animals were divided into five groups: CLP non-treated group, CLP-treated groups with bosentan, ambrisentan, and phosphoramidon (30, 5, and 0.5 mg/kg, respectively), and sham-operated group. In addition to the same set of groups, survival analysis was assigned Survival rate, histopathological assessment, and cardiorenal functions were analysed. Oxidant and antioxidant activities, ET-1, IL-6, and lactate were measured. The expression of TNF-α, p38, Klotho, and caspase-3 was evaluated by immunohistochemistry. CLP caused acute cardiorenal damage, high mortality, upregulated levels of ET-1, IL-6, and lactate, as well as an imbalance in oxidant/antioxidant activities, elevated expression of TNF-α, p38, caspase-3 and reduced expression of klotho. Bosentan, ambrisentan, or phosphoramidon improved survival, reduced the levels of inflammatory and oxidative stress parameters, improved cardiorenal functions and structure, elevated the tissue contents of GSH and SOD, raised the expression of klotho protein, and reduced the cardiorenal expression of p38, TNF-α and caspase-3. Endothelin receptor antagonists (ERAs); bosentan and ambrisentan, or endothelin converting enzyme inhibitor (ECE-i) phosphoramidon, are promising agents against sepsis-induced organ damage. This was evident in their cardiorenal protective effects, up-regulation of klotho, suppression of inflammation, oxidation, apoptosis, and enhancement of the antioxidant status.
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http://dx.doi.org/10.1111/1440-1681.70042 | DOI Listing |
Med Lett Drugs Ther
September 2025
Pharmaceuticals (Basel)
July 2025
Department of Health Statistics, College of Public Health, Chongqing Medical University, Chongqing 401331, China.
Pulmonary arterial hypertension (PAH) is a progressive and life-threatening disease. Adverse events (AEs) related to its drug treatment seriously damaged the patient's health. This study aims to clarify the causal relationship between PAH drugs and these AEs by combining pharmacovigilance signal detection with the Bayesian causal network model.
View Article and Find Full Text PDFCochrane Database Syst Rev
August 2025
Valley Health Pulmonary and Sleep Specialists, Winchester Medical Center, Winchester, Virginia, USA.
Rationale: Pulmonary arterial hypertension (PAH), a rare disorder, causes elevated pressure in the pulmonary arteries, leading to heart failure. Untreated PAH has a poor prognosis, emphasising the need for effective intervention. Pharmacological treatment includes pulmonary vasodilators such as endothelin receptor antagonists (ERA), prostacyclin analogues, phosphodiesterase type 5 inhibitors (PDE5i), and soluble guanylate cyclase stimulators, often used together to improve symptoms and quality of life while reducing mortality and risk of hospitalisation.
View Article and Find Full Text PDFPulm Circ
July 2025
Department of Pulmonology Clínica Imbanaco Grupo Quiron Salud Cali Colombia.
Pulmonary arterial hypertension (PAH) in intermediate-risk patients poses a challenge for clinicians, particularly in determining the optimal timing for escalating pharmacological treatment. We conducted a multicenter cross-sectional study that analyzed data from the Colombian Pulmonary Hypertension Network (HAPredCO) on patients diagnosed with PAH. Participants were stratified into low- and high-intermediate risk groups using the four-level ESC/ERS score, which incorporates optimized cutoff values for WHO functional class (WHO FC), the 6-min walk test (6MWT), and N-terminal pro-brain natriuretic peptide (NT-proBNP)/brain natriuretic peptide (BNP) concentration.
View Article and Find Full Text PDFRespir Med
July 2025
University of Arizona College of Medicine-Phoenix, Phoenix, AZ, USA; Banner - University Medical Center Phoenix, 1111 East McDowell Road, Phoenix, AZ 85006, USA. Electronic address:
Background: Few studies have evaluated macitentan alongside other endothelin receptor antagonists (ERAs) in patients with pulmonary arterial hypertension (PAH). This retrospective, observational, real-world, comparative effectiveness analysis assessed outcomes in PAH with macitentan versus other ERAs.
Methods: Adults (≥18 years) were included from the de-identified Optum Clinformatics Data Mart database (January 2014-December 2023).