Metabolic Syndrome Effects over Heart Tissue: A Histomorphological Glance under the Light of p97/VCP and SVIP
Metabolic syndrome(MetS) is a cluster of metabolic disorders that significantly increases the risk of heart disease and type 2 diabetes. p97/VCP (Valosin-Containing Protein), is an ATPase enzyme that regulates many vital processes in the cell such as cell cycle control, apoptosis, protein degradation, and cellular stress. Small VCP-interacting protein (SVIP) has various important functions in the cell which are particularly in the endoplasmic reticulum and proteasome systems. SVIP is a small but effective regulator of the protein recycling and quality control system in the cell. It affects processes such as cellular stress response, protein accumulation, and degradation, particularly through its interaction with the p97/VCP protein. MetS is one of the most important risk factors for cardiovascular diseases. However, the roles of p97/VCP and SVIP in cardiac tissue affected by MetS remain unclear. Therefore, this study aimed to investigate the histomorphological changes and the expression levels of p97/VCP and SVIP in rat heart tissue in a MetS model. The histomorphological alterations in heart tissues were evaluated using Hematoxylin-Eosin and Weigert Van Gieson staining methods. Using the immunohistochemical technique, the expression of p97/VCP and SVIP in rat heart tissue were examined. Statistical analyses were conducted and p
Authors
- Hilal Nakkaş (ORCID: https://orcid.org/0000-0003-0901-8875)
- Ayça Bilginoğlu (ORCID: https://orcid.org/0000-0002-1657-2607)
- Makbule Fulya Tutar Selcuk (ORCID: https://orcid.org/0000-0002-8961-9883)
- Şeyma Kipel (ORCID: https://orcid.org/0000-0002-4176-5136)
Institutions
- Rize Devlet Hastanesi (TR)
- Ankara Yıldırım Beyazıt University (TR)
Publication Details
- Journal
- Black Sea Journal of Health Science
- Published
- 2026-09-14
- DOI
- https://doi.org/10.19127/bshealthscience.1914438
- Primary Topic
- Endoplasmic Reticulum Stress and Disease
- Type
- article
- Field-Weighted Citation Impact
- 0.00