Targeting VDAC1 to protect against mitochondria-linked cell death pathways: apoptosis, pyroptosis, ferroptosis, and associated diseases
⁺ levels, preserved mitochondrial-associated hexokinase, and inhibited assembly/activation of the NLRP3 inflammasome. In Alzheimer's disease and inflammatory bowel disease mouse models, VBIT-4 and VBIT-12, respectively, protected against apoptosis, pyroptosis, ferroptosis, and disease-associated pathologies. Thus, we show that VDAC1 oligomerization represents a prime target for VBIT-4 and VBIT-12 that can simultaneously inhibit various PCD forms and diseases associated with enhanced PCD and/or inflammation.
Authors
- Sweta Trishna (ORCID: https://orcid.org/0000-0001-7757-0288)
- Anna Shteinfer-Kuzmine
- Varda Shoshan-Barmatz
- A. Karunanithi Nivedita
- J. Pan
- M. Santhanam
- R. W. Swerdlow
Institutions
- Ben-Gurion University of the Negev (IL)
- University of Florida (US)
- University of Kansas Medical Center (US)
Publication Details
- Journal
- APOPTOSIS
- Published
- 2026-04-01
- DOI
- https://doi.org/10.1007/s10495-025-02217-7
- Citations
- 1
- Primary Topic
- Ferroptosis and cancer prognosis
- Type
- article
- Field-Weighted Citation Impact
- 22.04
Funders
- Ben-Gurion University of the Negev