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牙周炎加速射血分数保留的小鼠心力衰竭进展

Periodontitis Accelerates Progression of Heart Failure With Preserved Ejection Fraction in Mice.

作者信息

Daana Samar, Rokach Yair, Abedat Suzan, Nachman Dean, Mohsen Hadeya, Karram Sama, Zandberg Yael, Tzach-Nachman Rinat, Cohen Jonathan, Amir Offer, Houri-Haddad Yael

机构信息

Cardiovascular Research Center, Heart Institute, Hadassah Medical Center, Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel.

Department of Prosthodontics, Hadassah Medical Center, Faculty of Dental Medicine, Hebrew University of Jerusalem, Jerusalem, Israel.

出版信息

JACC Basic Transl Sci. 2025 Aug;10(8):101270. doi: 10.1016/j.jacbts.2025.03.002. Epub 2025 Jun 11.

Abstract

Chronic low-grade inflammation and nitric oxide (NO) depletion are important contributors to heart failure with preserved ejection fraction (HFpEF) pathophysiology. Periodontitis (PD) is a common inflammatory disease implicated in dysregulation of NO hemostasis. Epidemiological studies have shown an association between PD and increased risk of cardiovascular disease, including heart failure. However, a causative relationship between the 2 diseases has not yet been proven. In this study, we sought to investigate the direct effect of PD induction on HFpEF progression in a mouse model. Induction of PD in HFpEF mice resulted in significant oral microbial dysbiosis, accelerated progression of diastolic dysfunction by echocardiography, and increased myocardial inflammation and fibrosis. These deleterious effects seen with PD were shown to be mediated by increased systemic blood pressure, increased systemic inflammation, and NO depletion. Our study provides evidence of potential mechanistic links between PD and HFpEF progression and suggests PD as a new therapeutic target for HFpEF.

摘要

慢性低度炎症和一氧化氮(NO)耗竭是射血分数保留的心力衰竭(HFpEF)病理生理学的重要促成因素。牙周炎(PD)是一种常见的炎症性疾病,与NO止血调节异常有关。流行病学研究表明,PD与包括心力衰竭在内的心血管疾病风险增加之间存在关联。然而,这两种疾病之间的因果关系尚未得到证实。在本研究中,我们试图在小鼠模型中研究PD诱导对HFpEF进展的直接影响。在HFpEF小鼠中诱导PD导致明显的口腔微生物群落失调、超声心动图显示舒张功能障碍加速进展,以及心肌炎症和纤维化增加。PD所见的这些有害影响被证明是由全身血压升高、全身炎症增加和NO耗竭介导的。我们的研究提供了PD与HFpEF进展之间潜在机制联系的证据,并表明PD是HFpEF的一个新的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b830/12399157/34c35e832f1a/ga1.jpg

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