Impact of myeloid differentiation protein 1 on cardiovascular disease

Jiang, Xiaobo; Ning, Peng; Yan, Fang; Wang, Jianfeng; Cai, Wei; Yang, Fan

doi:10.1016/j.biopha.2022.114000

Cited by 1 publication

(1 citation statement)

References 143 publications

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“…The pathophysiological factors driving the development of cardiomyopathy in diabetes include inflammation, apoptosis, oxidative stress, and fibrosis [27], [28]. Meanwhile, previous studies have shown that MD1 plays an important protective role in the development of cardiac disease by negatively regulating these processes [22], [23], [29]. In this study, we first demonstrated that the protein levels of MD1 in mice with DCM were significantly lower than those in WT mice.…”

Section: Discussionmentioning

confidence: 99%

Loss of MD1 Promotes Inflammatory and Apoptotic Atrial Remodelling in Diabetic Cardiomyopathy by Activating the TLR4/NF-κB Signalling Pathway

Shi¹,

Wang²,

Peng³

et al. 2023

Pharmacology

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Introduction: Myeloid differentiation protein 1 (MD1), a negative regulator of toll-like receptor 4 (TLR4), is widely expressed in the heart. Recent studies have shown that MD1 plays an important role in cardiac remodelling. However, the effects and potential mechanisms underlying MD1-mediated atrial remodelling in diabetic cardiomyopathy (DCM) remain unclear. Therefore, this study was designed to explore the role of MD1 in DCM-related atrial remodelling. Methods: MD1 knockout (MD1-KO) mice and wild-type (WT) littermates were injected with streptozotocin (STZ) to establish a diabetic mouse model. These mice were then used to evaluate MD1 expression and its effects on atrial remodelling in vivo. Results: MD1 expression was significantly decreased in STZ-induced diabetic mice. The loss of MD1 aggravated atrial fibrosis, inflammation, and apoptosis in DCM mice and promoted atrial remodelling. MD1-KO diabetic mice also showed higher susceptibility to atrial fibrillation (AF) and worse cardiac function. Mechanistically, the deletion of MD1 promoted the activation of the TLR4/NF-κB signalling pathway, resulting in atrial remodelling in DCM mice via increased p65 phosphorylation. Conclusions: The deletion of MD1 plays an important role in inflammatory and apoptotic atrial remodelling and increases susceptibility to AF in DCM mice, providing a new target for the preventive treatment of DCM-related atrial remodelling.

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