Non-alcoholic fatty liver disease (NAFLD) affects an estimated 25% of the global adult population and represents a spectrum from simple steatosis (fat accumulation) to non-alcoholic steatohepatitis (NASH) to fibrosis and cirrhosis. The progression from NAFLD to NASH is driven by chronic liver inflammation — the primary target of MSC therapy.
How MSCs Act on the Liver
Anti-Inflammatory Action
MSCs secrete IL-10 and TGF-β, suppressing liver inflammation. Critically, they regulate the balance between pro-inflammatory (M1) and anti-inflammatory (M2) liver macrophages (Kupffer cells), shifting the immune response toward tissue repair. They also inhibit NF-κB, a key signaling pathway driving oxidative stress and pro-inflammatory cytokine release (TNF-α, IL-6, IL-1β) in NAFLD.
Anti-Fibrotic Effects
Liver fibrosis — the scarring that drives cirrhosis — is mediated by activated hepatic stellate cells. MSCs inhibit hepatic stellate cell activation and release antifibrotic factors that promote breakdown of existing scar tissue. In animal models of NAFLD/NASH, MSC administration consistently reduces liver fibrosis scores.
Hepatocyte Regeneration
MSCs can differentiate into hepatocyte-like cells under appropriate conditions, and their paracrine secretions support existing hepatocyte survival and proliferation. Growth factors secreted by MSCs (VEGF, HGF) also improve liver vascularity, which is often impaired in fibrotic liver disease.
Who Is a Candidate
NAFLD patients in the NASH or early fibrosis stage (F0–F2 on biopsy or MRI elastography) are the best candidates. Patients with advanced cirrhosis (F4) or hepatic failure are not suitable for this intervention and require evaluation for transplant options. NAFLD often co-occurs with T2D, metabolic syndrome, or obesity — your full metabolic picture is assessed on the evaluation call.