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已发表论文
腹主动脉瘤中信号通路的治疗靶向：从发病机制到精准医疗
Authors Shaikh II, Singh S, Feng Y, Shahzad KA , Wang J, Zhou Q, Wang S , Zeng C, Shao C
Received 27 August 2025
Accepted for publication 21 December 2025
Published 31 December 2025 Volume 2025:19 Pages 12077—12111
DOI https://doi.org/10.2147/DDDT.S563581
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Leonidas Panos
Imran Ibrahim Shaikh,1,* Shekhar Singh,1,2,* Yuling Feng,3 Khawar Ali Shahzad,4 Jianfeng Wang,1 Quan Zhou,1 Shuanghu Wang,1 Chunlai Zeng,1,2 Chuxiao Shao5
1Central Laboratory of The Lishui Hospital of Wenzhou Medical University, The First Affiliated Hospital of Lishui University, Lishui People’s Hospital, Lishui, Zhejiang, 323000, People’s Republic of China; 2Department of Cardiology, Central Laboratory of The Lishui Hospital of Wenzhou Medical University, The First Affiliated Hospital of Lishui University, Lishui People’s Hospital, Lishui, Zhejiang, 323000, People’s Republic of China; 3Department of Vascular Surgery, Central Laboratory of The Lishui Hospital of Wenzhou Medical University, The First Affiliated Hospital of Lishui University, Lishui People’s Hospital, Lishui, Zhejiang, 323000, People’s Republic of China; 4Department of ORL-HNS, Shanghai Fourth People’s Hospital, School of Medicine, Tongji University, Shanghai, People’s Republic of China; 5School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325035, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Chuxiao Shao, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325035, People’s Republic of China, Tel +8619905880652, Email chuxiaoshao2000@126.com; scx1818@126.com Chunlai Zeng, Department of Cardiology, Central Laboratory of The Lishui Hospital of Wenzhou Medical University, Lishui People’s Hospital, The First Affiliated Hospital of Lishui University, Lishui, Zhejiang, 323000, People’s Republic of China, Email zengchunlai788@126.com; zengchunlai788710@lsu.edu.cn
Abstract: Abdominal aortic aneurysms (AAAs) are life-threatening cardiovascular disorders with limited treatment options, largely due to an incomplete understanding of their molecular and cellular pathogenesis. A comprehensive elucidation of the mechanisms driving AAA initiation, progression, and rupture is critical for developing novel therapeutic interventions. Emerging research has highlighted the central role of inflammatory processes in AAA pathophysiology, including dysregulated extracellular matrix (ECM) remodeling, chronic vascular inflammation, immune cell infiltration, and vascular smooth muscle cell (VSMC) dysfunction. These pathological processes are regulated by complex signaling pathways with divergent roles in AAA progression: while NF-κB, MAPK, STAT, and Notch signaling exacerbate disease pathogenesis, AMPK, PPAR-γ, and Nrf2 pathways exert protective effects. Notably, the PI3K/Akt and TGF-β signaling cascades demonstrate context-dependent dual roles, capable of either promoting or inhibiting AAA development. This comprehensive review synthesizes current knowledge of AAA pathophysiology with emphasis on druggable targets within these signaling networks. We critically evaluate emerging therapeutic strategies including miRNA-based interventions, nanoparticle-mediated drug delivery systems, and stem cell therapies that offer promising approaches for precision modulation of disease-specific pathways. By integrating current mechanistic understanding with therapeutic development, this review aims to provide a framework for designing effective pharmacological strategies that could transform AAA management from surgical intervention to medical prevention, addressing a critical unmet clinical need.
Keywords: abdominal aortic aneurysm, extracellular matrix remodeling, inflammation, vascular smooth muscle cell dysfunction, cellular signaling, therapeutic targets
1Central Laboratory of The Lishui Hospital of Wenzhou Medical University, The First Affiliated Hospital of Lishui University, Lishui People’s Hospital, Lishui, Zhejiang, 323000, People’s Republic of China; 2Department of Cardiology, Central Laboratory of The Lishui Hospital of Wenzhou Medical University, The First Affiliated Hospital of Lishui University, Lishui People’s Hospital, Lishui, Zhejiang, 323000, People’s Republic of China; 3Department of Vascular Surgery, Central Laboratory of The Lishui Hospital of Wenzhou Medical University, The First Affiliated Hospital of Lishui University, Lishui People’s Hospital, Lishui, Zhejiang, 323000, People’s Republic of China; 4Department of ORL-HNS, Shanghai Fourth People’s Hospital, School of Medicine, Tongji University, Shanghai, People’s Republic of China; 5School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325035, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Chuxiao Shao, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325035, People’s Republic of China, Tel +8619905880652, Email chuxiaoshao2000@126.com; scx1818@126.com Chunlai Zeng, Department of Cardiology, Central Laboratory of The Lishui Hospital of Wenzhou Medical University, Lishui People’s Hospital, The First Affiliated Hospital of Lishui University, Lishui, Zhejiang, 323000, People’s Republic of China, Email zengchunlai788@126.com; zengchunlai788710@lsu.edu.cn
Abstract: Abdominal aortic aneurysms (AAAs) are life-threatening cardiovascular disorders with limited treatment options, largely due to an incomplete understanding of their molecular and cellular pathogenesis. A comprehensive elucidation of the mechanisms driving AAA initiation, progression, and rupture is critical for developing novel therapeutic interventions. Emerging research has highlighted the central role of inflammatory processes in AAA pathophysiology, including dysregulated extracellular matrix (ECM) remodeling, chronic vascular inflammation, immune cell infiltration, and vascular smooth muscle cell (VSMC) dysfunction. These pathological processes are regulated by complex signaling pathways with divergent roles in AAA progression: while NF-κB, MAPK, STAT, and Notch signaling exacerbate disease pathogenesis, AMPK, PPAR-γ, and Nrf2 pathways exert protective effects. Notably, the PI3K/Akt and TGF-β signaling cascades demonstrate context-dependent dual roles, capable of either promoting or inhibiting AAA development. This comprehensive review synthesizes current knowledge of AAA pathophysiology with emphasis on druggable targets within these signaling networks. We critically evaluate emerging therapeutic strategies including miRNA-based interventions, nanoparticle-mediated drug delivery systems, and stem cell therapies that offer promising approaches for precision modulation of disease-specific pathways. By integrating current mechanistic understanding with therapeutic development, this review aims to provide a framework for designing effective pharmacological strategies that could transform AAA management from surgical intervention to medical prevention, addressing a critical unmet clinical need.
Keywords: abdominal aortic aneurysm, extracellular matrix remodeling, inflammation, vascular smooth muscle cell dysfunction, cellular signaling, therapeutic targets