ArticleInternational journal of molecular sciences2023
The Novel Compound SUL-138 Counteracts Endothelial Cell and Kidney Dysfunction in Sepsis by Preserving Mitochondrial Function.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- A Novel Hypothermic Preservation Formulation Containing SUL-138 Enables Long-Term Hypothermic Storage of Clinical-Grade CAR-T Cells.Pharmaceutics · 2026Article
- Hydroxysafflor yellow A attenuates sepsis-induced intestinal barrier dysfunction by modulating Bcl-2/SOD2-mediated mitochondrial apoptosis.Frontiers in pharmacology · 2026Article
- Mitochondria-Targeted Antioxidants Prevent Tachypacing-Induced Contractile Dysfunction in In Vitro Cardiomyocyte and In VivoAntioxidants (Basel, Switzerland) · 2025Article
- SUL-138 mitigates accelerated endothelial aging and protects the kidney.Clinical science (London, England : 1979) · 2025Article
- Targeting the Electron Transport System for Enhanced Longevity.Biomolecules · 2025Review
- Hibernation science harnessed to treat obesity and modify metabolism.Nature medicine · 2024Article
- Safety, tolerability and toxicokinetics of the novel mitochondrial drug SUL-138 administered orally to rat and minipig.Toxicology reports · 2024Article
- Restoring the infected powerhouse: Mitochondrial quality control in sepsis.Redox biology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Sepsis is defined as a dysregulated host response leading to organ dysfunction, which may ultimately result in the patient's death. Mitochondrial dysfunction plays a key role in developing organ dysfunction in sepsis. In this study, we explored the efficacy of the novel mitochondrial protective compound, SUL-138, in sepsis models in HUVECs and mice. In LPS-challenged HUVECs, SUL-138 preserved mitochondrial membrane potential and oxygen consumption and limited mitochondrial oxidative stress, resulting in increased survival at 48 h. Further, SUL-138 dampened the LPS-induced expression of IL-1β, but not of NLRP3, and IL-18 in HUVECs. Sepsis in mice induced by cecal ligation and puncture (CLP) led to a lower mitochondrial membrane potential and increased levels of mitochondrial oxidative stress in the kidney, which SUL-138 limited. In addition, SUL-138 mitigated the CLP-induced increase in kidney dysfunction markers NGAL and urea. It dampened the rise in kidney expression of IL-6, IL-1β, and ICAM-1, but not TNF-α and E-selectin. Yet, SUL-138 limited the increase in plasma levels of IL-6 and TNF-α of CLP mice. These results demonstrate that SUL-138 supports mitochondrial function, resulting in a limitation of systemic inflammation and preservation of kidney function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.