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Purine adducts as a presumable missing link for aristolochic acid nephropathy-related cellular energy crisis, potential anti-fibrotic prevention and treatment.

Gordana KocicMihajlo GajicKatarina TomovicJovan Hadzi-DjokicMarko AnderluhAndrija Smelcerovic
Published in: British journal of pharmacology (2021)
Aristolochic acid nephropathy is a progressive exposome-induced disease characterized by tubular atrophy and fibrosis culminating in end-stage renal disease and malignancies. The molecular mechanisms of the energy crisis as a putative cause of fibrosis have not yet been elucidated. In light of the fact that aristolochic acid forms DNA and RNA adducts by covalent binding of aristolochic acid metabolites to exocyclic amino groups of (deoxy)adenosine and (deoxy)guanosine, we hypothesize here that similar aristolochic acid adducts may exist with other purine-containing molecules. We also provide new insights into the aristolochic acid-induced energy crisis and presumably a link between already known mechanisms. In addition, an overview of potential targets in fibrosis treatment is provided, which is followed by recommendations on possible preventive measures that could be taken to at least postpone or partially alleviate aristolochic acid nephropathy.
Keyphrases
  • public health
  • chronic kidney disease
  • end stage renal disease
  • transcription factor
  • systemic sclerosis
  • high glucose
  • cell free
  • climate change
  • circulating tumor
  • drug induced
  • dna binding
  • human serum albumin