PhD Scientific Days 2026

Poster Session 2.Q - Cardiovascular Medicine and Research

Damages to the sarco/endoplasmic reticulum-mitochondria interaction in a type-2 myocardial infarction model

Name of the presenter

Farkas, Erika

Institute/workplace of the presenter

Department of Pharmacology and Pharmacotherapy

Authors

MSc Erika Farkas¹
1: Department of Pharmacology and Pharmacotherapy

Text of the abstract

Introduction
Myocardial infarction is a leading cause of death worldwide. Type-2 myocardial infarction is caused by non-atherothrombotic events leading to critical imbalance between oxygen supply and demand. Many cellular functions damaged in the disease are regulated by signalling between the sarco/endoplasmic reticulum (SR/ER) and mitochondria. This requires close physical contacts between the two organelles which is mediated by tethering proteins, the ER membrane protein vesicle-associated membrane protein-associated protein B (VAPB) and the outer mitochondrial membrane protein, protein tyrosine phosphatase interacting protein 51 (PTPIP51). A key function of VAPB-PTPIP51 tethering is to promote calcium delivery from the SR/ER stores to mitochondria. This calcium communication involves in some extent the inositol 1,4,5-trisphosphate (IP3) receptor in the SR/ER and the voltage-dependent anion-selective channel (VDAC) in mitochondria.
Aims
Our aim was to investigate whether VAPB–PTPIP51-mediated tethering is disrupted during type-2 myocardial infarction and whether calcium signaling between the IP3R and the VDAC is altered in this condition.
Methods
Type-2 myocardial infarction was induced in mice by isoprenaline treatment. Cardiac function was assessed in vivo by echocardiography. Hearts sections of the animals were examined by protein–protein interactions between VAPB and PTPIP51, as well as between IP3R and VDAC, using proximity ligation assay.
Result
In our type-2 myocardial infarction model, cardiac function was significantly deteriorated compared to controls. We observed a marked increase in VAPB–PTPIP51-mediated ER–mitochondria tethering, also the calcium signaling-associated interaction between the IP3R and the VDAC was significantly enhanced.
Conclusion
In an isoprenaline-induced type-2 myocardial infarction model VAPB–PTPIP51-mediated ER–mitochondria tethering and IP3R–VDAC-associated calcium signaling were significantly increased.
Funding
The János Bolyai Research Fellowship of the Hungarian Academy of Sciences (BO/00277/23/5) and the National Research, Development, and Innovation Office (NKFIH) of Hungary (FK146163).


Erika Farkas
farkas.erika@semmelweis.hu
Semmelweis University
Supervisor: Dr. Gábor Mórotz