Dysregulations in Cardiogenic Mechanisms by TGF-beta and Angiotensin II in Cardiac Remodeling Post-Ischemic Injury: a systematic review

Ovais Shafi, Kashaf Zahra, Haider Hussain Shah
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Abstract

Objective: The objective of this study is to look into how TGF-beta and Angiotensin II disrupt cardiogenic regulators (Isl1, Brg1/Baf60-Smarcd3 complex, Nkx2-5, GATA4, Tbx5, Mef2c, HAND1/2, MYOCD, MSX2, HOPX, Wnt-signaling pathway, Notch, FGF, BMPs) during cardiac remodeling post-ischemic injury. Background: Cardiac remodeling post-ischemic injury, influenced by TGF-beta and Angiotensin II, disrupts critical cardiogenic regulators essential for heart function. Understanding these disruptions is crucial for developing targeted therapies and biomarkers to assess disease severity. This research addresses a crucial gap in cardiovascular treatment by focusing on mechanisms underlying remodeling processes, aiming to improve therapeutic strategies and outcomes for ischemic heart disease patients. Methods: Databases, including PubMed, MEDLINE, Google Scholar, and open access/ subscription based journals were searched for published articles without any date restrictions, to look into how TGF beta and Angiotensin II disrupt cardiogenic regulators in cardiac remodeling post-ischemic. Based on the criteria mentioned in the methods section, studies were systematically reviewed with focus on objectives of the study. This study adheres to relevant PRISMA guidelines (Preferred Reporting Items for Systematic Reviews and Meta-Analyses). Results: Cardiac remodeling post-ischemic injury involves complex disruptions of cardiogenic regulators, prominently influenced by TGF-beta and Angiotensin II. Our study reveals these factors significantly alter critical regulators like Isl1, Nkx2.5, and GATA4, impacting myocardial repair mechanisms. TGF-beta induces fibrosis and inflammatory responses, while Angiotensin II exacerbates hypertrophic pathways and oxidative stress. Interactions between these pathways amplify remodeling through Smad, MAPK, and other signaling cascades. These findings point to the crucial roles of TGF-beta and Angiotensin II in pathological cardiac remodeling, highlighting potential targets for therapeutic interventions. Conclusion: Cardiac remodeling post-ischemic injury, influenced by TGF-beta and Angiotensin II, disrupts vital cardiogenic regulators like Isl1, Brg1/Baf60/Smarcd3 complex, Nkx2.5, GATA4, Tbx5, Mef2c, HAND1/2, MYOCD, MSX2, HOPX, Wnt-signaling pathway, Notch, FGF, and BMPs. These disruptions, involving altered receptor expression, signaling pathway interference, hypertrophic responses, and fibrosis promotion, compromise cardiac development and repair mechanisms. Targeting these pathways could enhance therapeutic strategies for ischemic heart disease by restoring normal regulator function and promoting effective cardiac repair and regeneration, thereby improving clinical outcomes.
缺血性损伤后心脏重塑过程中 TGF-beta 和血管紧张素 II 对心源性机制的失调:系统性综述
目的:本研究旨在探讨 TGF-beta 和血管紧张素 II 如何在缺血损伤后心脏重塑过程中破坏心源性调节因子(Isl1、Brg1/Baf60-Smarcd3 复合物、Nkx2-5、GATA4、Tbx5、Mef2c、HAND1/2、MYOCD、MSX2、HOPX、Wnt 信号通路、Notch、FGF、BMPs)。背景:缺血损伤后的心脏重塑受 TGF-beta 和血管紧张素 II 的影响,破坏了对心脏功能至关重要的关键心源性调节因子。了解这些干扰对于开发靶向疗法和评估疾病严重程度的生物标记物至关重要。这项研究关注重塑过程的内在机制,旨在改善缺血性心脏病患者的治疗策略和疗效,从而填补心血管治疗领域的重要空白:方法:在包括PubMed、MEDLINE、Google Scholar和开放获取/订阅期刊在内的数据库中搜索已发表的文章,没有任何日期限制,以研究TGF beta和血管紧张素II如何破坏缺血后心脏重塑过程中的心源性调节因子。根据 "方法 "部分中提到的标准,对研究进行了系统性审查,重点关注研究目标。结果:缺血损伤后的心脏重塑涉及复杂的心源性调节因子干扰,主要受 TGF-beta 和血管紧张素 II 的影响。我们的研究发现,这些因素极大地改变了Isl1、Nkx2.5和GATA4等关键调节因子,影响了心肌修复机制。TGF-beta诱导纤维化和炎症反应,而血管紧张素II则加剧肥大途径和氧化应激。这些途径之间的相互作用通过 Smad、MAPK 和其他信号级联扩大了重塑。这些研究结果表明了 TGF-beta 和血管紧张素 II 在病理性心脏重塑中的关键作用,突出了治疗干预的潜在靶点。结论:缺血损伤后的心脏重塑受到 TGF-beta 和血管紧张素 II 的影响,破坏了重要的致心调节因子,如 Isl1、Brg1/Baf60/Smarcd3 复合物、Nkx2.5、GATA4、Tbx5、Mef2c、HAND1/2、MYOCD、MSX2、HOPX、Wnt 信号通路、Notch、FGF 和 BMPs。这些干扰涉及受体表达改变、信号通路干扰、肥大反应和纤维化促进,损害了心脏发育和修复机制。以这些通路为靶点,可恢复正常调节器功能,促进有效的心脏修复和再生,从而改善临床疗效,从而加强缺血性心脏病的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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