<p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is an increasing global health challenge closely linked to obesity and the metabolic syndrome. This review explores the role of aldosterone as a central contributor to metabolic dysfunction, highlighting its association with adipose tissue dysfunction and systemic insulin resistance which can further influence MASLD development and progression. While aldosterone-related organ damage has been extensively studied in other contexts such as kidney disease, its involvement in MASLD has received less attention. Beyond classical renin-angiotensin-aldosterone system activation, aldosterone secretion can be directly stimulated by leptin and other adipogenic factors, creating a pathogenic link between obesity and metabolic impairment. Aldosterone amplifies chronic inflammation, oxidative stress and insulin resistance, primarily through mineralocorticoid receptor (MR)-dependent mechanisms. These involve both genomic actions regulating pro-inflammatory genes and rapid non-genomic signalling. Additionally, aldosterone MR-independent effects, can further contribute to oxidative stress and inflammatory responses. Significantly, the MR is expressed in liver cells, including hepatocytes, liver sinusoidal endothelial cells, Kupffer cells, and hepatic stellate cells. This expression can allow for direct aldosterone-mediated effect on hepatic inflammation, oxidative stress, and fibrosis, which can occur alongside or independently of systemic metabolic pathways. Such direct mechanisms may explain associations found in clinical studies correlating high aldosterone levels -even with low renin- with the prevalence and progression of MASLD. Recognizing aldosterone as a pleiotropic hormone that integrates metabolic and hepatic disease offers new insights into the cardio-kidney-metabolic syndrome and underscores the potential for targeted therapies.</p>