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Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease (NAFLD), is a chronic, progressive condition affecting about 38% of the global population and is strongly associated with features of the metabolic syndrome, including obesity and type 2 diabetes mellitus. MASLD is caused by a build-up of fat in the liver and includes a range of disease states, from isolated lipid accumulation or steatosis (metabolic dysfunction-associated steatotic liver, MASL) through to its active inflammatory form, metabolic dysfunction-associated steatohepatitis (MASH). Persistence of MASH leads, in some cases, to cirrhosis (scarring of the liver), liver failure and liver cancer. In 2022, the World Health Organization reported that obesity and overweight, which are strong independent risk factors for MASLD, affect almost 60% of adults and nearly one in three children in Europe. With its increasing prevalence rate, MASLD is becoming the most common indication for liver transplantation and the main underlying aetiology for the development of liver cancer. From a clinical perspective, the challenge is to identify which patients with MASLD will eventually progress to cirrhosis, end-stage liver disease, or liver cancer, so that appropriate care can be provided. At present, MASLD diagnosis requires a liver biopsy, which is invasive and can only be done in specialist hospitals, so there is a need for better non-invasive tools.
We welcome submission of primary research focused on MASLD. We encourage submission of manuscripts dealing with the prevention, diagnosis, management and monitoring of MASLD, including studies on biomarkers, non-invasive tests, pathology, therapies and dietary/lifestyle interventions. We welcome submission of translational studies in animal models, computational studies (for example digital pathology), and public health and epidemiology. Other article types, such as Reviews, Perspectives, and Comments that add significant insight will also be considered for inclusion in the Collection. All submissions will be subject to the same review process and editorial standards as regular Communications Medicine Articles.
Ivancovsky-Wajcman et al. outline the need for a holistic preventive hepatology approach, involving social nutrition and social prescribing, to address the public health threat of metabolic dysfunction-associated steatotic liver disease (MASLD). They argue that this will facilitate individuals’ engagement in behavioural modifications to treat MASLD.
Stähli, Becchetti, Korta Martiartu et al. present a first-in-human evaluation of computed ultrasound tomography in echo mode to quantify the speed of sound in the liver. Estimated values show an excellent discriminative ability in distinguishing normal versus steatotic livers, with potential value in the non-invasive diagnosis of liver steatosis.
Tsouka et al. compare metabolic signatures of metabolic dysfunction-associated steatohepatitis in a diet- and chemical-induced mouse model with human disease. By evaluating perturbations in enzymatic reactions via transcriptomics-driven metabolic pathway analysis, they observe similar alterations in lipid metabolism between the mouse model and humans.
Iwadare et al. investigate the value of serum autotaxin levels in predicting liver-related events within a retrospective cohort of 309 biopsy-proven NAFLD patients. Multivariate Cox proportional hazards models identify autotaxin levels and advanced fibrosis as independent predictive factors.