ArticleFrontiers in physiology2024
Deletion of Sigmar1 leads to increased arterial stiffness and altered mitochondrial respiration resulting in vascular dysfunction.
Article in Frontiers in physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Salidroside attenuates myocardial ischemia‑reperfusion‑induced oxidative stress and ferroptosis by promoting USP11‑mediated deubiquitination of PRDX2.International journal of molecular medicine · 2026Article
- Diquat-induced organ toxicity: a focus on regulated cell death pathways and mitochondrial dysfunction.Frontiers in cell and developmental biology · 2026Review
- Immunoelectron microscopy: a comprehensive guide from sample preparation to high-resolution imaging.Discover nano · 2025Review
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Authors and funding
11 authors.
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Abstract
Sigmar1 is a ubiquitously expressed, multifunctional protein known for its cardioprotective roles in cardiovascular diseases. While accumulating evidence indicate a critical role of Sigmar1 in cardiac biology, its physiological function in the vasculature remains unknown. In this study, we characterized the expression of Sigmar1 in the vascular wall and assessed its physiological function in the vascular system using global Sigmar1 knockout (Sigmar1
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