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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

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Canagliflozin Inhibits Palmitic Acid-Induced Vascular Cell Aging In Vitro through ROS/ERK and Ferroptosis Pathways.

Fang Wan^1,2, Xin He^1,2,3, Weidong Xie^1,2,3

¹State Key Laboratory of Chemical Oncogenomics, Shenzhen International Graduate School, Tsinghua University, Shenzhen 518055, China.

Antioxidants (Basel, Switzerland)

|July 27, 2024

Summary

This summary is machine-generated.

Canagliflozin (CAN) protects against high-fat-induced vascular aging by inhibiting ROS/ERK and ferroptosis pathways. This reveals new mechanisms for preventing cardiovascular disease and developing future lipid-lowering therapies.

Keywords:

ROS/ERK canagliflozin ferroptosis senescence

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Area of Science:

Cardiovascular Science
Cellular Aging
Pharmacology

Background:

Vascular aging contributes significantly to cardiovascular disease incidence.
High-fat diets are key inducers of vascular cell aging.
Canagliflozin (CAN), an SGLT2 inhibitor, shows cardiovascular benefits, but its mechanism remains unclear.

Purpose of the Study:

To investigate the effects of CAN on palmitic acid (PA)-induced vascular aging.
To elucidate the underlying mechanisms of CAN's anti-aging effects in vascular cells.
To explore the roles of ROS/ERK and ferroptosis pathways in lipid-induced vascular aging.

Main Methods:

Establishment of a vascular aging model using palmitic acid (PA).
Treatment of the aging model with Canagliflozin (CAN).
Analysis of ROS/ERK and ferroptosis signaling pathways.

Main Results:

CAN effectively alleviates PA-induced vascular cell aging.
CAN inhibits the activation of ROS/ERK signaling pathways.
CAN suppresses ferroptosis signaling pathways in aged vascular cells.

Conclusions:

CAN demonstrates protective effects against lipid-induced vascular aging.
Inhibition of ROS/ERK and ferroptosis pathways is a key mechanism for CAN's action.
Findings offer novel insights into vascular aging and potential therapeutic strategies.