Aug 2026· In vitro Cellular & Developmental Biology-Animal· 0 citations· 42 references
Medicine
TL;DR
A novel regulatory pathway involving FTO, m⁶A, PRTN3, and CXCL9/CXCR3 in CAD pathogenesis is uncovered, highlighting FTO as a promising target for therapeutic intervention.
The RNA methyltransferase zinc finger CCCH-type containing protein 13 (ZC3H13) is downregulated in atherosclerosis (AS), but its functional mechanism remains unclear. Endothelial-mesenchymal transition (EndMT) is a core pathological driver of endothelial dysfunction in AS. This study aimed to investigate the biological...
Chen Wang, Ying Xing, L.-V. Wang et al.· Molecular and Cellular Biolo...· 0 citations
The present study demonstrated that the m6A demethylase fat mass and obesity-associated (FTO) regulates autophagy, lipid metabolism and plaque vulnerability by targeting autophagy related 5 (ATG5).
Feng-Xian Guo, Mei He, Yao-Nan Li et al.· Molecular Medicine Reports· 0 citations
It is indicated that FSTL1 represents a promising immunomodulatory target and highlight its potential as a therapeutic target to reprogram the immunosuppressive microenvironment and improve the efficacy of GC immunotherapy.
Ming Yang, Rong-Fei Wang, Xiao Wang et al.· Journal of Translational Med...· 0 citations
BACKGROUND
FTO (fat mass and obesity-associated) protein, a key N6-methyladenosine demethylase, plays a critical role in cardiovascular disease. However, its function in vascular calcification remains poorly understood.
METHODS
High phosphate (Pi) was used to induce calcification in vascular smooth muscle cells (VSMC...
Yu-Chen Xie, Huan Zhao, Lan Lan et al.· Arteriosclerosis, Thrombosis...· 0 citations
The STING-ZBP1 signaling cascade is established as a central regulator of macrophage PANoptosis during atherogenesis and a previously unrecognized mechanism linking innate immune signaling to inflammatory cell death in atherosclerosis is uncovered, highlighting this pathway as a promising therapeutic target for atheros...
Hong Zhou, Yue-Qing Han, Danmei Liu et al.· Cell Death & Disease· 0 citations
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