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Global Translational Medicine ECM receptor pathway in endotheliocytes after MI

content detection. In addition, RNA interference will be methods and targets that can alleviate late reactive fibrosis
employed to reduce the expression of a targeted protein while preserving the early scar repair process.
within the cell line, while overexpression of the target
protein will allow us to identify changes in the expression Acknowledgments
of other related proteins within the target pathway. This None.
approach aims to clarify whether Col6α2, Vtn, and Itgβ3
exert their effects through the ECM-receptor interaction Funding
pathway. Furthermore, empirical testing will be conducted This work was financially supported by the National
to determine whether inhibitors of the target proteins can Key Research and Development Program of China
induce changes in the fibrotic phenotype. This evaluation (2022YFB3807300); the second Tibetan Plateau
will involve assessing the degree of fibrosis in an animal Scientific Expedition and Research Program (STEP)
model of cardiac fibrosis following MI. In the future, a (2019QZKK0606); Clinical Cohort Construction Program
comprehensive understanding of the interplay between the of Peking University Third Hospital (BYSYDL2022005);
ECM and ECs during the cardiac fibrosis process will be and Key Clinical Projects of Peking University Third
attained by conducting meticulous analyses of cardiac ECs Hospital (BYSYZD2023006).
at various junctures post-MI. This effort will contribute
to the construction of a more comprehensive interaction Conflict of interest
network atlas.
The authors declare they have no competing interests.
In this study, we isolated primary ECs from MI mice and
analyzed their profiles of differential protein expression. Author contributions
Our findings highlight the significant involvement of Conceptualization: Lingyun Zu
the ECM receptor pathway in regulating ECs post-MI. Formal analysis: Xuan Wu, Jiageng Cai
However, it is essential to note that the verification of Investigation: Xuan Wu, Jiageng Cai, Peng Wang
the ECM receptor in the MI mouse model has not been Methodology: Xuan Wu, Jiageng Cai
conducted, representing a critical aspect that requires Writing – original draft: Xuan Wu
further supplementation and refinement in subsequent Writing – review & editing: Xuan Wu, Jiageng Cai, Lingyun Zu
research conducted by our group.

5. Conclusion Ethics approval and consent to participate
The animal ethics of this project have been approved by
ECs potentially contribute to cardiac fibrosis post-MI by Peking University Third Clinical Medical School Ethical
regulating ECM-receptor interaction. While this study Committee of Animals (LA2022077).
successfully verified the target proteins through Western
blot, further validation in both in vivo and in vitro settings Consent for publication
is crucial to unravel underlying mechanisms. The precise
mechanism of action remains unclear, forming a key Not applicable.
focus for the next phase of experimental planning. In the
context of cardiac fibrosis, accurately selecting sampling Availability of data
nodes and understanding their protective or adverse Not applicable.
effects on the heart after MI is essential. The definition of
time points within different stages of the fibrotic reaction References
represents a time range, necessitating the examination 1. Frangogiannis NG, 2014, The inflammatory response in
of multiple time nodes to study the dynamic changes of myocardial injury, repair, and remodelling. Nat Rev Cardiol,
TMT-related proteins. However, achieving a comparison 11: 255–265.
of multiple time nodes is challenging due to the associated https://doi.org/10.1038/nrcardio.2014.28
requirement for a large sample size. In our study, we
initially selected the 2-week post-MI time node for high- 2. Yuan Y, Zhang Y, Han X, et al., 2017, Relaxin alleviates
throughput screening of TMT quantitative proteomics. TGFβ1-induced cardiac fibrosis via inhibition of Stat3-
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of multiple nodes for further verification. The purpose
of this study is to identify a molecular pathway capable of https://doi.org/10.1016/j.bbrc.2017.09.110
inhibiting fibrosis development post-MI without interfering 3. Francis Stuart SD, De Jesus NM, Lindsey ML, et al., 2015,
with protective mechanisms. The goal is to explore treatment The crossroads of inflammation, fibrosis, and arrhythmia

Volume 2 Issue 4 (2023) 11 https://doi.org/10.36922/gtm.2217