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L-type calcium channel blockers decrease the iron overload-mediated oxidative stress in renal epithelial cells by

Linfeng Sun1, Xiaoding Lin2, Sakorn Pornprasert3

  • 1Department of Physiology, School of Basic Medical Sciences, Southwest Medical University, Luzhou, 646000, China.

European Journal of Pharmacology
|September 8, 2020
PubMed
Summary
This summary is machine-generated.

L-type calcium channel (LTCC) blockers reduce kidney cell damage from iron overload by decreasing iron uptake and enhancing iron transport. These findings suggest LTCC blockers as a potential treatment for iron overload-related kidney injury.

Keywords:
Iron overloadL-type calcium channelNifedipineOxidative stressRenal epithelial cellsVerapamil

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Area of Science:

  • Nephrology
  • Cardiovascular Pharmacology
  • Cell Biology

Background:

  • Iron-mediated oxidative stress is a primary driver of chronic kidney injury.
  • L-type calcium channel (LTCC) blockers have demonstrated protective effects against iron overload in various cell types, but their role in kidney cells remains under-investigated.
  • The exact mechanisms by which LTCC blockers influence iron transport in the kidneys are not fully understood.

Purpose of the Study:

  • To investigate the efficacy of LTCC blockers (nifedipine and verapamil) in mitigating iron overload-induced oxidative stress and apoptosis in renal epithelial cells.
  • To elucidate the underlying mechanisms of LTCC blocker action on cellular iron transport and accumulation in kidney cells.

Main Methods:

  • Utilized HK-2 and HEK293 cell lines exposed to ferric ammonium citrate to model iron overload.
  • Administered nifedipine and verapamil to assess their effects on oxidative stress, apoptosis, and cellular iron content.
  • Quantified the expression levels of key iron transport proteins, including divalent metal transporter 1 (DMT1), divalent metal transporter ZIP14, and ferroportin1 (FPN1).

Main Results:

  • Nifedipine and verapamil treatments significantly decreased oxidative stress and apoptosis in ferric ammonium citrate-treated cells (P < 0.05).
  • LTCC blockers reduced cellular iron content and prevented the iron level increase induced by ferric ammonium citrate.
  • These blockers upregulated the expression of DMT1, ZIP14, and FPN1 in HK-2 cells, and FPN1 in HEK293 cells.

Conclusions:

  • LTCC blockers effectively alleviate iron overload-induced oxidative stress and apoptosis in renal epithelial cells.
  • The protective effects are attributed to the modulation of iron transport, including reduced iron uptake and enhanced iron export, thereby decreasing cellular iron accumulation.
  • LTCC blockers represent a promising therapeutic strategy for preventing or treating kidney injury associated with primary or secondary iron overload.