# MASLD als systeemziekte: lever, hart en nier verstrengeld door metabole cross-talk

*geplaatst 2026-09-13 · Nierziekte · Current hypertension reports · doi 10.1007/s11906-026-01388-1 · https://hartvaat.nl/2026/09/04/masld-als-systeemziekte-lever-hart-en-nier-verstrengeld-door-metabole-cross-talk/*

Deze narratieve review beschrijft hoe metabole dysfunctie-geassocieerde leverziekte (MASLD) fungeert als systeemziekte die hart en nier beschadigt via lipotoxiciteit, ontsteking en verstoorde hepatokine-signalering (zoals BDNF en NGF). Hoewel metabole therapieën zoals GLP-1-receptoragonisten en SGLT2-remmers al klinisch bewezen effecten hebben op lever- en metabole uitkomsten, blijft onduidelijk in hoeverre hun cardiovasculaire en renale voordelen voortkomen uit directe weefselbescherming versus secundaire metabole verbetering. Het in kaart brengen van specifieke hepatokineprofielen biedt een beloftevolle route voor nieuwe biomarkers en therapeutische targets, maar vereist verder klinisch onderzoek om de vertaalslag naar de dagpraktijk te maken.

## English: The Cardio-Renal-Hepatic Axis in MASLD. Role of BDNF, NGF, and Metabolic Cross-Talk.

This narrative review examines how metabolic dysfunction-associated steatotic liver disease (MASLD) acts as a systemic driver of cardiorenal dysfunction, primarily through lipotoxicity, epicardial inflammation, and dysregulated hepatokine signaling (e.g., BDNF, NGF, FGF19/21). While metabolic therapies like GLP-1 receptor agonists and SGLT2 inhibitors already improve hepatic and metabolic outcomes, their direct versus indirect cardiorenal protective mechanisms require further clinical validation. Profiling specific hepatokine signatures may eventually yield novel biomarkers and therapeutic targets, but routine clinical application awaits prospective trials.

## Abstract (original, from the publication)

PURPOSE OF REVIEW: To evaluate the crosstalk between the liver, heart, and kidneys in metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH), highlighting the distinct regulatory roles of non-traditional hepatokines, and to assess shared therapeutic targets and molecular mechanisms driving cardiorenal complications in MASLD patients. RECENT FINDINGS: Emerging evidence highlights that hepatic lipid accumulation drives cardiac damage, which manifests as adverse remodeling, diastolic dysfunction, and coronary microvascular dysfunction. These abnormalities are mediated primarily by systemic lipotoxicity, inflammation of epicardial adipose tissue, and a pro-thrombotic environment. Mechanistically, altered hepatokine signaling mediates systemic cross-talk. Specifically, the downregulation of cardioprotective and renoprotective brain-derived neurotrophic factor (BDNF) and the dual metabolic roles of nerve growth factor (NGF), fibroblast growth factor (FGF) 19, and FGF21 accelerate the progression of both heart failure and chronic kidney disease (CKD). Concurrently, metabolic therapies such as glucagon-like peptide-1 (GLP-1) receptor agonists, sodium-glucose cotransporter-2 (SGLT2) inhibitors, and peroxisome proliferator-activated receptor (PPAR) agonists demonstrate significant efficacy in ameliorating steatosis, inflammation, and overall metabolic outcomes. MASLD acts as a systemic driver of multi-organ dysfunction within the cardio-renal-hepatic axis. Profiling specific hepatokine signatures offers a promising frontier for identifying novel therapeutic targets and biomarkers of disease acceleration. Furthermore, while current metabolic therapies show remarkable potential, rigorous clinical testing remains critical to definitively determine whether their cardiovascular and renal benefits stem from direct tissue-specific protective mechanisms or secondary metabolic improvements.

Auteurs: Lucy C Taylor, Michael I Adenawoola, Claire B Wingfield, Maren K Nadolski, David E Stec

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Bron: Current hypertension reports, https://doi.org/10.1007/s11906-026-01388-1. Bijgewerkt 2026-09-06T01:14:14Z. Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.