ArticleJournal of the American Society of Nephrology : JASN2015
Stanniocalcin-1 inhibits renal ischemia/reperfusion injury via an AMP-activated protein kinase-dependent pathway.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 82 citations in OpenAlex.
- Stanniocalcin-1 and -2: The insulin-like growth factor system and beyond.Molecular biology reports · 2026Review
- Deletion of Megalin in Kidney Tubular Epithelium Up-Regulates TGFβ1 Signaling, Aggravates Ischemia/Reperfusion Kidney Injury, and Accelerates the Progression to Chronic Kidney Disease.The American journal of pathology · 2026Article
- Advances in understanding the role of mitochondria in renal ischemia-reperfusion injury.Clinical and experimental nephrology · 2025Review
- AAV-mediated STC-1 expression mitigates neuroinflammation and preserves visual function in degenerative retinopathy.Journal of translational medicine · 2025Article
- Biphasic protective effects of macrophage migration inhibitory factor in ischemia/reperfusion-induced acute kidney injury.Communications biology · 2025Article
- Sirtuins and Resveratrol in Cardiorenal Diseases: A Narrative Review of Mechanisms and Therapeutic Potential.Nutrients · 2025Review
- Stanniocalcin-1: A Novel Mediator in Diabetic Kidney Disease and Cardiovascular Disease.Kidney international reports · 2025Review
- Roles of SIRT3 in aging and aging-related diseases.International journal of biological sciences · 2025Review
- Emerging role and the signaling pathways of uncoupling protein 2 in kidney diseases.Renal failure · 2024Review
- Variants in tubule epithelial regulatory elements mediate most heritable differences in human kidney function.Nature genetics · 2024Article
- Sirtuins in kidney health and disease.Nature reviews. Nephrology · 2024Review
- Maresin-1 Attenuates Sepsis-Associated Acute Kidney Injury via Suppressing Inflammation, Endoplasmic Reticulum Stress and Pyroptosis by Activating the AMPK/SIRT3 Pathway.Journal of inflammation research · 2024Article
- Sirtuins in kidney homeostasis and disease: where are we now?Frontiers in endocrinology · 2024Review
- Stanniocalcin 1 promotes lung metastasis of breast cancer by enhancing EGFR-ERK-S100A4 signaling.Cell death & disease · 2023Article
- Importance of Mitochondria in Cardiac Pathologies: Focus on Uncoupling Proteins and Monoamine Oxidases.International journal of molecular sciences · 2023Review
- Identification and characterization of a membrane receptor that binds to human STC1.Life science alliance · 2022Article
- Interactions between leucines within the signal peptides of megalin and stanniocalcin-1 are crucial for regulation of mitochondrial metabolism.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Adipose-derived stem cells alleviate liver injury induced by type 1 diabetes mellitus by inhibiting mitochondrial stress and attenuating inflammation.Stem cell research & therapy · 2022Article
- Correlation between coenzyme QBioImpacts : BI · 2022Article
- Megalin-Mediated Trafficking of Mitochondrial Intracrines: Relevance to Signaling and Metabolism.Journal of cellular immunology · 2021Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
AKI is associated with increased morbidity, mortality, and cost of care, and therapeutic options remain limited. Reactive oxygen species are critical for the genesis of ischemic AKI. Stanniocalcin-1 (STC1) suppresses superoxide generation through induction of uncoupling proteins (UCPs), and transgenic overexpression of STC1 inhibits reactive oxygen species and protects from ischemia/reperfusion (I/R) kidney injury. Our observations revealed high AMP-activated protein kinase (AMPK) activity in STC1 transgenic kidneys relative to wild-type (WT) kidneys; thus, we hypothesized that STC1 protects from I/R kidney injury through activation of AMPK. Baseline activity of AMPK in the kidney correlated with the expression of STCs, such that the highest activity was observed in STC1 transgenic mice followed (in decreasing order) by WT, STC1 knockout, and STC1/STC2 double-knockout mice. I/R in WT kidneys increased AMPK activity and the expression of STC1, UCP2, and sirtuin 3. Inhibition of AMPK by administration of compound C before I/R abolished the activation of AMPK, diminished the expression of UCP2 and sirtuin 3, and aggravated kidney injury but did not affect STC1 expression. Treatment of cultured HEK cells with recombinant STC1 activated AMPK and increased the expression of UCP2 and sirtuin 3, and concomitant treatment with compound C abolished these responses. STC1 knockout mice displayed high susceptibility to I/R, whereas pretreatment of STC1 transgenic mice with compound C restored the susceptibility to I/R kidney injury. These data suggest that STC1 is important for activation of AMPK in the kidney, which mediates STC1-induced expression of UCP2 and sirtuin 3 and protection from I/R.
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