Chronic low-grade inflammation in heart failure with preserved ejection fraction.
Chronic low-grade inflammation in heart failure with preserved ejection fraction.
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DOI：
10.1111/acel.13453
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发表时间：
2021-09
期刊：
影响因子：
7.8
通讯作者：
Ibrahim A
中科院分区：
文献类型：
--
作者：
Mesquita T;Lin YN;Ibrahim A
心力衰竭（HF）伴保留射血分数（HFpEF）是目前心衰的主要形式，其风险随着年龄的增长而急剧增加。随着年龄增长而发生的低度炎症（称为“炎症”）是HFpEF病理的共同特征。抑制促炎途径与HFpEF疾病严重程度的减轻和更好的预后相关。从这个角度来看，炎症小体信号在介导慢性炎症和心血管疾病进展中起着核心作用。然而，炎症体-免疫信号轴与HFpEF年龄依赖性进展之间的因果关系仍然是推测性的。在这篇综述中，我们总结了目前对炎症途径在年龄依赖性心功能下降中的作用的理解。我们还将评估HFpEF病理生理学中炎症途径的最新进展和证据，特别关注炎症小体信号。心力衰竭伴射血分数保留（HFpEF）是一种以多系统疾病为特征的复杂综合征。尽管年龄依赖性患病率越来越高，但有效的治疗方法却很少。目前被认为是心血管疾病中最大的未满足的医疗需求，合并症驱动的炎症已成为HFpEF发病机制的关键组成部分。因此，慢性低度炎症可能驱动HFpEF的关键病理生理变化。
Heart failure (HF) with preserved ejection fraction (HFpEF) is currently the predominant form of HF with a dramatic increase in risk with age. Low‐grade inflammation, as occurs with aging (termed “inflammaging”), is a common feature of HFpEF pathology. Suppression of proinflammatory pathways has been associated with attenuated HFpEF disease severity and better outcomes. From this perspective, inflammasome signaling plays a central role in mediating chronic inflammation and cardiovascular disease progression. However, the causal link between the inflammasome‐immune signaling axis on the age‐dependent progression of HFpEF remains conjectural. In this review, we summarize the current understanding of the role of inflammatory pathways in age‐dependent cardiac function decline. We will also evaluate recent advances and evidence regarding the inflammatory pathway in the pathophysiology of HFpEF, with special attention to inflammasome signaling. Heart failure (HF) with preserved ejection fraction (HFpEF) is a complex syndrome characterized by multisystem disorders. Despite the increasing age‐dependent prevalence, there are very few effective therapies. Considered now as the greatest unmet medical need in cardiovascular disease, comorbidity‐driven inflammation has emerged as a critical component of HFpEF pathogenesis. Thus, chronic low‐grade inflammation may drive key pathophysiological changes in HFpEF.
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影响因子：
4
作者：
Campisi, Judith
通讯作者：
Campisi, Judith
影响因子：
5.4
作者：
Abernethy A;Raza S;Sun JL;Anstrom KJ;Tracy R;Steiner J;VanBuren P;LeWinter MM
通讯作者：
LeWinter MM
DOI：
10.3390/antiox9090860
发表时间：
2020-09-14
期刊：
Antioxidants (Basel, Switzerland)
影响因子：
--
作者：
Bode D;Wen Y;Hegemann N;Primessnig U;Parwani A;Boldt LH;M Pieske B;R Heinzel F;Hohendanner F
通讯作者：
Hohendanner F
DOI：
10.1146/annurev-pathol-121808-102144
发表时间：
2010
期刊：
Annual review of pathology
影响因子：
--
作者：
Coppé JP;Desprez PY;Krtolica A;Campisi J
通讯作者：
Campisi J
SUMO介导的NLRP3调节调节炎症体活性。
影响因子：
16.6
作者：
Barry R;John SW;Liccardi G;Tenev T;Jaco I;Chen CH;Choi J;Kasperkiewicz P;Fernandes-Alnemri T;Alnemri E;Drag M;Chen Y;Meier P
通讯作者：
Meier P