PKM2

Meng Hao, Xutong Yan, Yexiang Jiang, Wenwen Li, Zeyuan Cao, Manjin Zhang, Peiyi Li, Can Li, Songtao Shi

Hospital of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, South China Center of Craniofacial Stem Cell Research, Guangdong Provincial Key Laboratory of Stomatology, Guangzhou, 510055, China. · pubmed

Paper

Abstract

Chronic periodontitis (CP) is one of the most prevalent local inflammatory disorders and is associated with various systemic diseases. However, the relationship between local CP pathogenesis and systemic metabolic responses is not fully elucidated. In this study, we show that CP causes systemic inflammation, leading to apoptotic resistance and senescent cell accumulation, which are crucial for maintaining local inflammation in a CP mouse model. Eliminating senescent cells through systemic senolytic therapy ameliorate local CP pathological changes. Proteomic analysis reveals that CP patient plasma extracellular vesicles show upregulation of immune response-related proteins and downregulation of metabolic and apoptosis-related proteins, among which pyruvate kinase M2 (PKM2) was significantly reduced. Moreover, CP mice show reduced circulating apoptotic vesicles (apoVs), particularly those carrying PKM2. Systemic administration of PKM2

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Research summary

Chronic periodontitis leads to systemic inflammation and senescent cell accumulation, which can be ameliorated by senolytic therapy. The study addresses the connection between local inflammation and systemic metabolic responses, which is pertinent to understanding aging and age-related diseases.

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