When calcium crosstalk turns ferroptotic: the SERCA2-VDAC1 axis in AKI.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 42476679.
- Also identified by DOI 10.1016/j.kint.2026.05.005.
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Abstract
Organelle communication through endoplasmic reticulum-mitochondrial crosstalk is essential for maintaining cellular homeostasis and is tightly regulated by tethering proteins within mitochondria-associated endoplasmic reticulum membranes. In a recent study published in Kidney International, He et al. identified sarcoplasmic/endoplasmic reticulum Ca<sup>2+</sup>-ATPase 2 as a key regulator of endoplasmic reticulum-mitochondrial calcium homeostasis in proximal tubules and demonstrated that loss of sarcoplasmic/endoplasmic reticulum Ca<sup>2+</sup>-ATPase 2 drives voltage-dependent anion channel 1 oligomerization, mitochondrial DNA release, stimulator of interferon genes activation, and ferroptosis in acute kidney injury. This study establishes the sarcoplasmic/endoplasmic reticulum Ca<sup>2+</sup>-ATPase 2-voltage-dependent anion channel 1 axis as a mechanistic link between mitochondrial calcium dysregulation and ferroptotic tubular injury.
Medical subject headings
- Sarcoplasmic Reticulum Calcium-Transporting ATPases
- Calcium
- Acute Kidney Injury
- Voltage-Dependent Anion Channel 1
- Calcium Signaling
- Kidney Tubules, Proximal