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Article

S-nitrosylation of HINT1 in macrophages aggravates foam cell formation and atherosclerosis.

Redox biology - 1 Mar 2026

Tang Ke, Zheng Tianshu, Zhu Hao, Xu Fan, Ma Congcong, Qi Zhenhua, Cao Siyi, Da Qiang, Yan Ke, Wu Wencheng, Han Yi, Xie Liping, Zhang Yan, Ji Yong

Abstract excerpt

Atherosclerosis (AS) is the primary cause of most cardiovascular diseases, such as coronary artery disease (CAD), myocardial infarctions and strokes. S-nitrosylation (SNO), a prototypic redox-based posttranslational modification, is involved in cardiovascular diseases. Histidine triad nucleotide-binding protein 1 (HINT1) was identified S-nitrosylated at cysteine 84 (Cys84) in oxidized low-density lipoprotein...

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Topics

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Share to Active Transport, Cell Nucleus
Share to CD36 Antigens

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Exportin 1 Protein

Share to Foam Cells

Share to Lipoproteins, LDL

Share to Nitric Oxide Synthase Type II

Share to Scavenger Receptors, Class A

Share to Upstream Stimulatory Factors

Source

Open in PubMed Open full text

Identifiers

PMID: 41633223
DOI: 10.1016/j.redox.2026.104063
PMCID: PMC12886079

Genes

HINT1
CD36
CAD
LDLR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 24 Oct 2026.

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