Interference with mitochondrial function as part of the antifibrogenic effect of Rilpivirine: A step towards novel targets in hepatic stellate cell activation

Biomed Pharmacother. 2024 Sep:178:117206. doi: 10.1016/j.biopha.2024.117206. Epub 2024 Jul 29.

Abstract

Activated hepatic stellate cells (aHSCs), the main perpetrators of liver fibrosis, are a promising therapeutic target in the treatment of chronic liver disease. During liver injury, HSCs transcend from a quiescent to a fibrotic phenotype, a process which involves major metabolic reprogramming with altered mitochondrial function. The antiretroviral drug Rilpivirine (RPV) has demonstrated a hepatoprotective and specifically antifibrotic effect in several animal models of chronic liver injury, as well as in vitro. Herein, we use HSCs activated with the profibrogenic cytokine TGF-β to explore whether mitochondrial function is implicated in this effect. The mitochondrial bioenergetic profile, morphology and dynamics of TGF-β-treated cells (48 h) were altered and these effects were prevented by co-treatment with clinically relevant concentrations of RPV. A MitoStress Test (Seahorse Analyzer) revealed that TGF-β increased both oxygen consumption rate (basal respiration, maximal respiration and spare respiratory capacity) and extracellular acidification rate (indicative of increased glycolysis). Cells exposed to TGF-β also displayed diminished mitochondrial membrane potential and enhanced mitochondrial fission. All of these effects were rescued with RPV. RNA sequencing analysis of cells exposed to TGF-β revealed the presence of 338 differentially expressed genes that encode mitochondrial proteins (mito-DEGs), of which 139 and 199 were significantly up- and down-regulated (adjusted p<0.05). This alteration in 15 (10.79 %) and 31 (22.03 %) of the up-regulated and 16 (8.04 %) and 49 (24.62 %) of the down-regulated mitoDEGs was prevented with co-exposure to RPV 4μM or 8μM, respectively. In conclusion, alterations in mitochondrial function are implicated in the antifibrogenic action of RPV, pointing to potential novel antifibrotic targets.

Keywords: Hepatic stellate cells; Liver fibrosis; Mitochondria; Rilpivirine; TGF-β; Therapeutic targets.

MeSH terms

  • Animals
  • Antifibrotic Agents / pharmacology
  • Hepatic Stellate Cells* / drug effects
  • Hepatic Stellate Cells* / metabolism
  • Humans
  • Liver Cirrhosis / drug therapy
  • Liver Cirrhosis / metabolism
  • Liver Cirrhosis / pathology
  • Membrane Potential, Mitochondrial / drug effects
  • Mitochondria* / drug effects
  • Mitochondria* / metabolism
  • Mitochondrial Dynamics / drug effects
  • Oxygen Consumption / drug effects
  • Rilpivirine* / pharmacology
  • Transforming Growth Factor beta* / metabolism

Substances

  • Rilpivirine
  • Transforming Growth Factor beta
  • Antifibrotic Agents