3.3.1 Ferroptosis is involved in the pathophysiology of
hypertension
Existing studies have found that ferroptosis is involved in endothelial
cell dysfunction, which can lead to changes in vasomotor function and
cause hypertension11. Vascular smooth muscle cells
(VSMCs), as one of the main cellular components of the vascular wall,
can maintain the tension of the vascular wall through a slow and mild
contraction. The phenotypic transformation of VSMCs is closely related
to the pathophysiological process of hypertension. Recent studies have
found that ferroptosis can induce the transition of VSMCs from
contractile phenotype to synthetic phenotype90. This
suggests that ferroptosis is related to the pathogenesis of
hypertension.
Many studies have shown that ROS plays an important role in vascular
remodeling and endothelial dysfunction associated with hypertension.
Increased ROS can promote endothelial dysfunction, and accelerate VSMCs
proliferation and vascular remodeling, leading to vascular injury,
increased peripheral resistance, and elevated blood
pressure91,92. An important feature of ferroptosis is
an increase in intracellular ROS levels. A recent in vitro study found
that VSMC undergoes ferroptosis under high hydrostatic pressure,
accompanied by iron accumulation, increased ROS production, and lipid
peroxidation7.In addition, it has been proposed that
lenvatinib can induce ferroptosis in endothelial cells, which
subsequently leads to vascular dysfunction and
hypertension13. The above studies have proved that
ferroptosis is involved in the pathophysiology of hypertension.