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Restoration of mitochondrial Ca2+ and redox homeostasis by enhancement of SK channels rescues Ca2+ cycling in HFpEF cardiomyocytes
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DOI：10.1016/j.yjmcc.2026.05.004.png)
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Abstract
En 中文
• Mitochondrial Ca2+ overload promotes production of reactive oxygen species (ROS) thereby contributing to pro-arrhythmic disturbances in intracellular Ca2+ cycling in myocytes from ZSF1 rat hearts with diastolic dysfunction. • Pharmacological enhancement of mitochondrial small conductance Ca2+ activated K+ (SK) channels reverses mitochondrial Ca2+ overload, reducing mito-ROS and stabilizing intracellular Ca2+ cycling. • Activation of mito-SK channels reduces pathological Ca2+ accumulation in mitochondria of ZSF1 rat myocytes by promoting opening of low-conductance permeability transition pore openings, without deleterious effects on mitochondrial membrane potential and ATP production.
Keywords:
HFpEF
SK channels
Mitochondria
Ryanodine receptor
Calcium handling
DTDP
2,2′-dithiodipyridine
DTT
dithiothreitol
IMM
inner mitochondrial membrane
ISO
Isoproterenol
HFpEF
Heart failure with preserved ejection fraction
HFrEF
Heart failure with reduced ejection fraction
MICU
Mitochondrial calcium uptake protein
MCU
Mitochondrial Ca2+ uniporter
NCLX
Na+/Ca2+/Li+ exchanger
NCX1
Na+/Ca2+ exchanger type 1
PKA
Protein kinase A
PLB
Phospholamban
ROS
Reactive oxygen species
RyR2
Ryanodine receptor type 2
SCW
Spontaneous Ca2+ wave
SERCA2a
Sarcoplasmic endoplasmic reticulum Ca2+ ATPase type 2a
SK
Small conductance Ca2+ activated K+ channel
SR
Sarcoplasmic reticulum
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