2. Academic Validation
  3. Toll-like receptor 2 deficiency ameliorates obesity-induced cardiomyopathy via inhibiting NF-κB signaling pathway

Toll-like receptor 2 deficiency ameliorates obesity-induced cardiomyopathy via inhibiting NF-κB signaling pathway

  • Int Immunopharmacol. 2024 Jan 25:128:111551. doi: 10.1016/j.intimp.2024.111551.
Chenchen Qian 1,  Diyun Xu 2,  Jiong Wang 2,  Yue Luo 2,  Tianyang Jin 2,  Lijiang Huang 3,  Yafen Zhou 3,  Zhaohong Cai 3,  Bo Jin 2,  Hongdan Bao 4,  Yi Wang 5
Affiliations

Affiliations

  • 1 Joint Research Center on Medicine, The Affiliated Xiangshan Hospital of Wenzhou Medical University, Ningbo, Zhejiang, China; Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • 2 Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • 3 Joint Research Center on Medicine, The Affiliated Xiangshan Hospital of Wenzhou Medical University, Ningbo, Zhejiang, China.
  • 4 Joint Research Center on Medicine, The Affiliated Xiangshan Hospital of Wenzhou Medical University, Ningbo, Zhejiang, China. Electronic address: 410725066@qq.com.
  • 5 Joint Research Center on Medicine, The Affiliated Xiangshan Hospital of Wenzhou Medical University, Ningbo, Zhejiang, China; Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China; School of Pharmacy, Hangzhou Normal University, Hangzhou, Zhejiang, China. Electronic address: yi.wang1122@wmu.edu.cn.
PMID: 38278067 DOI: 10.1016/j.intimp.2024.111551
Abstract

Growing evidence demonstrates that chronic low-grade inflammation, which is induced by high-fat diet (HFD) or saturated fatty acid, plays an important role in the obesity-induced cardiomyopathy (OIC) process. Moreover, obesity is associated with the activation of different inflammatory pathways, including nuclear factor-κB (NF-κB), Toll-like-receptor-2 (TLR2) and Toll-like-receptor-4 (TLR4). In this study, we established an HFD-induced cardiac injury mouse model and palmitate (PA)-induced myocardial cell model to evaluate the role of TLR2 in OIC. Our data show that TLR2 blockade using TLR2 knockout (KO) mice or a TLR2-specific inhibitor, C29, markedly ameliorated HFD- or PA-induced inflammation, myocardial fibrosis, and hypertrophy both in vivo and in vitro. Moreover, the PA-induced myocardial cell injury was mediated via inducing the formation of TLR2-MyD88 complex in a TLR4-independent manner in cardiomyocytes. Our data prove the critical role of cardiac TLR2 in the pathogenesis of HFD- and saturated fatty acid-induced myocarditis, fibrosis, myocardial hypertrophy, and cardiac dysfunction. Inhibition of TLR2 pathway may be a therapeutic strategy of OIC.

Keywords

Cardiomyocyte; Inflammation; Obesity-induced cardiomyopathy; TLR2.

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