Loss of Hepatocyte-Specific RECK Exacerbates Metabolic Dysfunction-Associated Steatohepatitis.

Metabolic dysfunction-associated steatohepatitis (MASH) continues to be a major health crisis worldwide due to increases in obesity and insulin resistance. The role of the extracellular matrix regulator REversion Inducing Cysteine Rich Protein With Kazal Motifs (RECK) in metabolic liver disease is poorly understood. We previously reported that RECK gain-of-function, specifically in hepatocytes, protects against diet-induced MASH.

Outcomes and survival prediction in adults with sickle cell disease treated with extracorporeal membrane oxygenation.

The utility of extracorporeal membrane oxygenation (ECMO) support for adult patients with sickle cell disease (SCD) remains poorly understood. We aimed to characterize a cohort of adult individuals with SCD in the Extracorporeal Life Support Organization (ELSO) registry who underwent venoarterial (VA) or venovenous (VV) ECMO treatment, assess clinical outcomes for each modality and determine predictors of mortality. This multicenter, retrospective study evaluated in-hospital mortality and clinical outcomes such as bleeding and thrombotic events (BTE) of adult VA and VV ECMO ELSO registry patients with SCD associated ICD-9/10-CM codes.

A murine model of gestational diabetes reveals MASLD risk and alterations in markers of hepatic mitochondrial metabolism.

Introduction: Gestational Diabetes Mellitus (GDM) impacts roughly 1 in 7 pregnancies and results in metabolic dysfunction-associated steatotic liver disease (MASLD) in 30% of these women. Nonetheless, there exists a dearth of investigation into the relationship between GDM and MASLD. Here, we sought to investigate the potential role of hepatic mitochondrial function in GDM and MASLD.

Ketone metabolites in metabolic dysfunction-associated steatotic liver disease progression: optimizing keto-therapeutic strategies.

Metabolic dysfunction-associated steatotic liver disease (MASLD) ranges from simple steatosis to hepatocellular injury, inflammation, and fibrosis, ultimately leading to end-stage liver disease. Despite its rising prevalence, treatment options remain limited, highlighting the need for novel therapeutic strategies. In recent years, ketone metabolism has emerged as a key modulator of hepatic metabolic health.

Heterozygous R403Q mutation impairs left atrial mitochondrial function in a Yucatan mini-pig model of genetic nonobstructive hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) can be caused by a R403Q gene mutation, which drives pathological cardiac remodeling and may ultimately lead to heart failure. Here, we sought to examine the effects of this mutation on cardiac mitochondrial function in a Yucatan mini-pig model of genetic HCM. Activity of key mitochondrial enzymes, citrate synthase and β-hydroxyacyl-CoA dehydrogenase, was significantly reduced in the left atrium of HCM animals compared with the control group.