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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

Effects of μ-Agatoxin-Aa1a in Cellular and Rat Models of Myocardial Ischemia–Reperfusion Injury

  • Elena Iurova1
  • Dinara Dolgova2,3
  • Natalya Mikheeva2,4
  • Anna Ermakova1
  • Dmitrii Sugak1
  • Aigul Gilmutdinova1
  • Aleksandr Fomin1
  • Yury Saenko1,5
5 affiliations
  1. 1Laboratory of Research and Development of Peptide Drugs and Vaccines, S. P. Kapitsa Research Institute of Technology, Ulyanovsk State University, Ulyanovsk 432017, Russia
  2. 2Laboratory of Molecular and Cellular Biology, S. P. Kapitsa Research Institute of Technology, Ulyanovsk State University, Ulyanovsk 432017, Russia
  3. 3Department of Physiology and Pathophysiology, Ulyanovsk State University, Ulyanovsk 432017, Russia
  4. 4Department of Biology, Ecology and Environmental Management, Ulyanovsk State University, Ulyanovsk 432017, Russia
  5. 5Autonomous Non-Commercial Organization “Agency for Scientific and Technical Initiatives”, Ulyanovsk Ave. 13, Ulyanovsk 432067, Russia
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Abstract

Myocardial infarction is one of the common cardiovascular diseases. Sodium overload in the myocardium is another of the most important mechanisms underlying ischemia/reperfusion injury. Na+ entry into the cell through ion channels can be controlled using peptide toxins targeting ion channels. In our work, we analyze the use of mu-agatoxin-Aa1a, as a sodium channel modulator, as a cytoprotective agent in ischemia/reperfusion injury. For IRI modeling in vitro, the H9C2 culture was placed under oxygen-glucose deprivation conditions followed by reperfusion. Cell death and ion dynamics were recorded using a fluorescent plate reader. Reversible myocardial ischemia of rats in vivo was created by applying an occluder under the main branch of the left coronary artery. Histological and biochemical changes were recorded. The study demonstrated the ability of mu-agatoxin-Aa1a myocardial cells to adapt to rapidly changing extracellular conditions upon restoration of normal blood flow after a period of ischemia. Thus, the study allows us to consider mu-agatoxin-Aa1a as a biologically active molecule with a targeted effect to enhance the adaptation of cardiomyocytes to OGD/reperfusion conditions.

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Cite

BibTeXRIS
BibTeX
@article{iurova2026effects,
  title = {{Effects of μ-Agatoxin-Aa1a in Cellular and Rat Models of Myocardial Ischemia–Reperfusion Injury}},
  author = {Elena Iurova and Dinara Dolgova and Natalya Mikheeva and Anna Ermakova and Dmitrii Sugak and Aigul Gilmutdinova and Aleksandr Fomin and Yury Saenko},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = oct,
  doi = {10.3390/ijms27209287},
  url = {https://www.mdpi.com/1422-0067/27/20/9287},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Effects of μ-Agatoxin-Aa1a in Cellular and Rat Models of Myocardial Ischemia–Reperfusion Injury
AU  - Elena Iurova
AU  - Dinara Dolgova
AU  - Natalya Mikheeva
AU  - Anna Ermakova
AU  - Dmitrii Sugak
AU  - Aigul Gilmutdinova
AU  - Aleksandr Fomin
AU  - Yury Saenko
PY  - 2026
DA  - 2026/10/01
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27209287
UR  - https://www.mdpi.com/1422-0067/27/20/9287
AB  - Myocardial infarction is one of the common cardiovascular diseases. Sodium overload in the myocardium is another of the most important mechanisms underlying ischemia/reperfusion injury. Na+ entry into the cell through ion channels can be controlled using peptide toxins targeting ion channels. In our work, we analyze the use of mu-agatoxin-Aa1a, as a sodium channel modulator, as a cytoprotective agent in ischemia/reperfusion injury. For IRI modeling in vitro, the H9C2 culture was placed under oxygen-glucose deprivation conditions followed by reperfusion. Cell death and ion dynamics were recorded using a fluorescent plate reader. Reversible myocardial ischemia of rats in vivo was created by applying an occluder under the main branch of the left coronary artery. Histological and biochemical changes were recorded. The study demonstrated the ability of mu-agatoxin-Aa1a myocardial cells to adapt to rapidly changing extracellular conditions upon restoration of normal blood flow after a period of ischemia. Thus, the study allows us to consider mu-agatoxin-Aa1a as a biologically active molecule with a targeted effect to enhance the adaptation of cardiomyocytes to OGD/reperfusion conditions.
SN  - 1422-0067
ER  -