Cellular signallingJun 15, 2026

The body clock gene BMAL1 slows aging in gum cells to reduce worsening of diabetes-related gum disease

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Jun 20, 2026

Abstract

Diabetes significantly aggravated alveolar bone resorption and accelerated gingival fibroblast senescence in a mouse model of diabetes periodontitis.

A hyperglycemic environment exacerbates periodontal inflammation and tissue destruction.
Diabetes and periodontitis exhibit a complex bidirectional relationship that worsens both conditions.
High glucose and lipopolysaccharide exposure activates the JAK1-STAT3 signaling pathway in gingival fibroblasts.
Downregulation of brain and muscle ARNT-like 1 (BMAL1) is associated with gingival fibroblast senescence.
Pharmacological activation of BMAL1 may mitigate senescence and mitochondrial dysfunction in gingival fibroblasts.

Simplified

In a hyperglycemic environment, periodontal inflammatory responses and the destruction of periodontal supporting tissues are exacerbated, leading to a severe form of diabetes periodontitis (DPD). Diabetes and periodontitis exhibit a bidirectional relationship that significantly increases the complexity and severity of each condition. A key pathological feature in this process is the functional impairment of gingival fibroblasts (GFs) within the high-glucose inflammatory microenvironment. In this study, a DPD mouse model was established. It was found that diabetes significantly aggravated alveolar bone resorption and accelerated GFs senescence, which was accompanied by a marked downregulation of brain and muscle ARNT-like 1 (BMAL1) expression. Pharmacological activation of BMAL1 effectively mitigated GFs senescence and mitochondrial dysfunction, and consequently alleviated alveolar bone destruction in DPD mice. By simulating the high-glucose inflammatory microenvironment in vitro, we confirmed that the combination of high glucose (HG) and lipopolysaccharide (LPS) activates the JAK1-STAT3 signaling pathway, downregulates BMAL1, disrupts mitochondrial homeostasis, and ultimately induces GFs senescence. This study elucidates the pathological mechanism underlying GFs senescence in the high-glucose inflammatory microenvironment, thereby providing a novel perspective for the targeted therapy of DPD.

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Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

PubMed

The body clock gene BMAL1 slows aging in gum cells to reduce worsening of diabetes-related gum disease

Abstract

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Abstract

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