ArticleInternational journal of molecular sciences2020
IGF-1 Deficiency Rescue and Intracellular Calcium Blockade Improves Survival and Corresponding Mechanisms in a Mouse Model of Acute Kidney Injury.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Insulin-like growth factor-1/insulin-like growth factor-1 receptor signalling in macrophages facilitates recovery from acute lung injury.Annals of medicine · 2026Article
- Mitochondrial genomes of Mentha reveal structural complexity and evolutionary diversity.Molecular genetics and genomics : MGG · 2026Article
- The role of IGFBP-1 in the clinical prognosis and pathophysiology of acute kidney injury.American journal of physiology. Renal physiology · 2025Observational
- The effect ofTranslational andrology and urology · 2024Article
- Effect of IGF-1C domain-modified nanoparticles on renal ischemia-reperfusion injury in mice.Renal failure · 2022Article
- Combination therapy of insulin-like growth factor I and BTP-2 markedly improves lipopolysaccharide-induced liver injury in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Bioinformatics analysis of pathways of renal infiltrating macrophages in different renal disease models.Translational andrology and urology · 2021Article
- The Effects of Insulin-Like Growth Factor I and BTP-2 on Acute Lung Injury.International journal of molecular sciences · 2021Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study was undertaken to test two therapies for acute kidney injury (AKI) prevention, IGF-1, which is renal protective, and BTP-2, which is a calcium entry (SOCE) inhibitor. We utilized lipopolysaccharide (LPS) IP, as a systemic model of AKI and studied in five groups of animals. Three experiments showed that at 7 days: (1) LPS significantly reduced serum IGF-1 and intramuscular IGF-I in vivo gene therapy rescued this deficiency. (2) Next, at the 7-day time point, our combination therapy，compared to the untreated group,caused a significant increase in survival, which was noteworthy because all of the untreated animals died in 72 hrs. (3) The four pathways associated with inflammation, including (A) increase in cytosolic calcium, (B) elaboration of proinflammatory cytokines, (C) impairment of vascular integrity, and (D) cell injury, were adversely affected in renal tissue by LPS, using a sublethal dose of LPS. The expression of several genes was measured in each of the above pathways. The combined therapy of IGF-1 and BTP-2 caused a favorable gene expression response in all four pathways. Our current study was an AKI study, but these pathways are also involved in other types of severe inflammation, including sepsis, acute respiratory distress syndrome, and probably severe coronavirus infection.
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