Key result
Pharmacologic inhibition of lysyl oxidase with BAPN significantly reduced extracellular matrix deposition by 64.63% and ameliorated renal fibrosis after ischemic injury in mice.
Why the study?
Although serum LOX was recently found to be a potential diagnostic biomarker for renal fibrosis, the mechanism regulating LOX and its contribution to renal fibrosis remained unknown.
Population
Human kidney sections from patients with renal fibrosis alongside IRI, UUO, and FA animal models
Comparison
Pharmacologic inhibition of LOX with BAPN vs control in vivo
Design
Preclinical experimental and human tissue study
Authors
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LOX inhibition reduces fibrosis in animal ischemic injury models; leaves open translation to human renal disease.
p-value: p=<0.05
LOX plays an essential role in renal fibrosis by catalyzing collagen cross-linking, and its pharmacologic inhibition ameliorates fibrosis in preclinical models.
Zhang et al. (2022) studied Renal fibrosis. BAPN (β-aminopropionitrile) vs. Vehicle/saline was evaluated on Extracellular matrix (ECM) deposition (Masson trichrome-positive area) (p=<0.05). Pharmacologic inhibition of lysyl oxidase with BAPN significantly reduced extracellular matrix deposition by 64.63% and ameliorated renal fibrosis after ischemic injury in mice.
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