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Klotho attenuates D-galactose-induced cardiac aging through the ROS/NLRP3/pyroptosis pathway
Sui-Sui Wang1, Xu Zhang2, Ze-Zhi Ke3
1Department of Cardiology, First School of Clinical Medicine, The First Affiliated Hospital of Guangdong Pharmaceutical University, 19 Nonglinxia Road, Yuexiu District, Guangzhou 510080, PR China; Department of Nuclear Medicine, The Affiliated Guangdong Second Provincial General Hospital of Jinan University, No.466 Road Xingang, Guangzhou, Guangdong 510317, PR China.
Klotho protein protects against heart aging caused by D-galactose by regulating the ROS/NLRP3/pyroptosis pathway. This study reveals Klotho
Area of Science:
- Cardiovascular Biology
- Aging Research
- Molecular Mechanisms of Disease
Background:
- The NLRP3 inflammasome is implicated in cardiac aging.
- Klotho, an anti-aging protein, offers cardioprotection.
- D-galactose (D-gal) induces cardiac aging phenotypes.
Purpose of the Study:
- To investigate Klotho's protective effects on D-gal-induced cardiac aging.
- To elucidate the underlying molecular mechanisms involving the ROS/NLRP3/pyroptosis pathway.
Main Methods:
- Mice and H9C2 cardiomyocytes were treated with D-gal.
- Cardiac aging markers, oxidative stress, inflammation, and pyroptosis were assessed.
- Echocardiography and histopathology evaluated cardiac function and structure.
Main Results:
- Klotho treatment and NLRP3 knockout reduced D-gal-induced cardiac aging markers, inflammation, oxidative stress, and pyroptosis.
- Klotho improved cardiac function and attenuated cardiac remodeling.
- These effects were reversed by Nigericin, confirming pathway involvement.
Conclusions:
- Klotho effectively delays D-galactose-induced cardiac aging.
- The protective mechanism involves the regulation of the reactive oxygen species (ROS)/NLRP3/pyroptosis pathway.
- Klotho represents a potential therapeutic target for cardiac aging.
