Ghiasi Mohsen
Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran.
Heliyon. 2024 Nov 30;10(23):e40812. doi: 10.1016/j.heliyon.2024.e40812. eCollection 2024 Dec 15.
Heart failure (HF) syndrome is of great interest as an emerging epidemic. Due to the increasing elderly population worldwide, the total number of HF patients is increasing every day. This disease places a significant economic burden on the healthcare and treatment systems of developing societies, and this situation is very concerning. Despite many advances in the diagnosis and treatment of cardiovascular diseases, HF is still the main cause of death worldwide. This clinical syndrome has many cellular and molecular complications, which are often aggravated by increased levels of pro-inflammatory cytokines, which lead to adverse clinical outcomes. Nuclear factor kappa B (NF-κB), a pivotal family of transcription factors, plays a crucial role in various biological processes, particularly in inflammation, immune response, cell proliferation, and cell survival. Studies show that the NF-κB signaling pathway plays a role in modulating cardiac regeneration, apoptosis, and myocardial fibrosis. It has been found that the NF-κB signaling pathway can affect heart function and HF through the regulation of matrix metalloproteinases and fibrotic mediators. Also, the NF-κB pathway regulates cell activities in cardiac cardiomyocytes and regulates the function of this organ by establishing a precise interaction between apoptosis and pyroptosis. However, the exact molecular mechanisms of this influence have not been well defined and there are many scientific gaps in this matter. This review tries to highlights potential therapeutic strategies to target NF-κB, including the use of anti-inflammatory agents and genetic modulation, which may provide new ways to reduce cardiac fibrosis and improve outcomes in HF patients. Certainly, increasing understanding of the multifaceted role of NF-κB in HF can lead to innovative treatments aimed at reducing the growing number of patients worldwide.
心力衰竭（HF）综合征作为一种新出现的流行病备受关注。由于全球老年人口不断增加，HF患者总数每天都在上升。这种疾病给发展中社会的医疗保健和治疗系统带来了巨大的经济负担，这种情况令人十分担忧。尽管心血管疾病的诊断和治疗取得了许多进展，但HF仍然是全球主要的死亡原因。这种临床综合征有许多细胞和分子并发症，促炎细胞因子水平升高往往会加剧这些并发症，进而导致不良临床结局。核因子κB（NF-κB）是一个关键的转录因子家族，在各种生物过程中发挥着至关重要的作用，尤其是在炎症、免疫反应、细胞增殖和细胞存活方面。研究表明，NF-κB信号通路在调节心脏再生、细胞凋亡和心肌纤维化中发挥作用。已经发现，NF-κB信号通路可通过调节基质金属蛋白酶和纤维化介质来影响心脏功能和HF。此外，NF-κB途径调节心肌细胞中的细胞活动，并通过在细胞凋亡和焦亡之间建立精确的相互作用来调节该器官的功能。然而，这种影响的确切分子机制尚未明确界定，在这方面存在许多科学空白。本综述试图强调针对NF-κB的潜在治疗策略，包括使用抗炎药物和基因调节，这可能为减少心脏纤维化和改善HF患者的预后提供新方法。当然，对NF-κB在HF中多方面作用的深入了解可以带来旨在减少全球患者数量不断增加的创新治疗方法。
