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Peer-reviewedCC BYFrontiers in cardiovascular medicine

Ubiquitination regulation in coronary microcirculation dysfunction: focus on the endothelial cells.

  • Qingying Zhang1,2,3
  • Tingting Wang1,2,3
  • Siyu Wang1,2,3
  • Yushan Chen1,2
  • Yiwen Sheng1,2,3
  • Haodi Zhang1,2,3
  • Yunhao Wang1,2,3
  • Boyuan Jin1,2,3
  • Chengjun Hua1,2,3
  • Xinyi Han1,2,3
  1. 1Heart Center/National Regional (Traditional Chinese Medicine) Cardiovascular Diagnosis and Treatment Center, The First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, Henan, China.
  2. 2Department of Cardiology, The First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, Henan, China.
  3. 3The First Clinical Medical College, Henan University of Traditional Chinese Medicine, Zhengzhou, Henan, China.
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Abstract

Basic and clinical research on coronary microvascular disease (CMD) has spanned half a century. As a pathogenesis independent of epicardial coronary stenosis, CMD has become a major hotspot in cardiovascular medicine. Ubiquitination, a vital post-translational modification in eukaryotic cells, precisely regulates target proteins via the E1-E2-E3 enzymatic cascade and plays a critical role in cardiovascular homeostasis and pathophysiology. Recent evidence indicates that the ubiquitin-proteasome system (UPS) is deeply involved in the development of CMD by modulating nitric oxide production, barrier function, and inflammatory signaling in coronary microvascular endothelial cells. This review summarizes recent advances in ubiquitination, elaborates its molecular mechanisms in regulating coronary microcirculation, and dissects its pathogenic roles in diabetes, hypertension, and myocardial ischemia/reperfusion injury (MIRI).We further discuss potential therapeutic strategies and translational challenges of targeting the ubiquitination pathway for CMD, including proteasome inhibitors, E3 ligase modulators, deubiquitinase agonists, and PROTACs, aiming to provide new insights for future research.

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Cite

BibTeXRIS
BibTeX
@article{zhang2026ubiquitination,
  title = {{Ubiquitination regulation in coronary microcirculation dysfunction: focus on the endothelial cells.}},
  author = {Qingying Zhang and Tingting Wang and Siyu Wang and Yushan Chen and Yiwen Sheng and Haodi Zhang and Yunhao Wang and Boyuan Jin and Chengjun Hua and Xinyi Han},
  journal = {Frontiers in cardiovascular medicine},
  year = {2026},
  month = oct,
  doi = {10.3389/fcvm.2026.1952434},
  url = {https://europepmc.org/article/MED/42903409},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Ubiquitination regulation in coronary microcirculation dysfunction: focus on the endothelial cells.
AU  - Qingying Zhang
AU  - Tingting Wang
AU  - Siyu Wang
AU  - Yushan Chen
AU  - Yiwen Sheng
AU  - Haodi Zhang
AU  - Yunhao Wang
AU  - Boyuan Jin
AU  - Chengjun Hua
AU  - Xinyi Han
PY  - 2026
DA  - 2026/10/06
JO  - Frontiers in cardiovascular medicine
DO  - 10.3389/fcvm.2026.1952434
UR  - https://europepmc.org/article/MED/42903409
AB  - Basic and clinical research on coronary microvascular disease (CMD) has spanned half a century. As a pathogenesis independent of epicardial coronary stenosis, CMD has become a major hotspot in cardiovascular medicine. Ubiquitination, a vital post-translational modification in eukaryotic cells, precisely regulates target proteins via the E1-E2-E3 enzymatic cascade and plays a critical role in cardiovascular homeostasis and pathophysiology. Recent evidence indicates that the ubiquitin-proteasome system (UPS) is deeply involved in the development of CMD by modulating nitric oxide production, barrier function, and inflammatory signaling in coronary microvascular endothelial cells. This review summarizes recent advances in ubiquitination, elaborates its molecular mechanisms in regulating coronary microcirculation, and dissects its pathogenic roles in diabetes, hypertension, and myocardial ischemia/reperfusion injury (MIRI).We further discuss potential therapeutic strategies and translational challenges of targeting the ubiquitination pathway for CMD, including proteasome inhibitors, E3 ligase modulators, deubiquitinase agonists, and PROTACs, aiming to provide new insights for future research.
SN  - 2297-055X
ER  -