ArticleRedox biology2020
Salusin-β mediates tubular cell apoptosis in acute kidney injury: Involvement of the PKC/ROS signaling pathway.
Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 62 citations in OpenAlex.
- Oocyte-specific knockout of eIF2B subunits causes apoptosis of mouse oocytes within the early growing follicles via DNA damage and mitochondrial dysfunction.Cell death & disease · 2026Article
- Oocyte-specific knockout of eIF2 subunits causes apoptosis of mouse oocytes within the early growing follicles via mitochondrial dysfunctions and DNA damage.Cell death & disease · 2026Article
- Pre-CRRT furosemide and mortality in sepsis-associated AKI: A retrospective cohort study.PloS one · 2026Article
- Baicalin alleviates sepsis-associated acute kidney injury through activation of the PPAR-γ/UCP1 signaling pathway.Renal failure · 2025Article
- Inhibition of PGK1 ameliorates acute kidney injury through inactivating the PKM2/ALOX12/ferroptosis pathway in a study with male mice.Nature communications · 2025Article
- Therapeutic Potential of Apocynin: A Promising Antioxidant Strategy for Acute Kidney Injury.Antioxidants (Basel, Switzerland) · 2025Review
- Effects of Peptides and Bioactive Peptides on Acute Kidney Injury: A Review Study.Iranian biomedical journal · 2025Review
- Sodium pump subunit NKAα1 protects against diabetic endothelial dysfunction by inhibiting ferroptosis through the autophagy-lysosome degradation of ACSL4.Clinical and translational medicine · 2025Article
- Tear and blood salusin-α, and -β, copeptin, and asprosin in patients with glaucoma and ocular hypertension.Arquivos brasileiros de oftalmologia · 2025Article
- HACE1 as a bridge between oxidative stress and autophagy.Frontiers in immunology · 2025Review
- Fe-flavonoid nanozyme as dual modulator of oxidative stress and autophagy for acute kidney injury repair.Theranostics · 2025Article
- CHIP drives proteasomal degradation of NUR77 to alleviate oxidative stress and intrinsic apoptosis in cisplatin-induced nephropathy.Communications biology · 2024Article
- Downregulation of salusins alleviates hypertrophic cardiomyopathy via attenuating oxidative stress and autophagy.European journal of medical research · 2024Article
- Berberine alleviates ischemia reperfusion injury induced AKI by regulation of intestinal microbiota and reducing intestinal inflammation.BMC complementary medicine and therapies · 2024Article
- Mutational burden of XPNPEP3 leads to defects in mitochondrial complex I and cilia in NPHPL1.iScience · 2023Article
- Serum salusin-β levels in patients with systemic lupus erythematosus.Clinical rheumatology · 2023Article
- Sodium butyrate enhances titanium nail osseointegration in ovariectomized rats by inhibiting the PKCα/NOX4/ROS/NF-κB pathways.Journal of orthopaedic surgery and research · 2023Article
- Article
- NDUFV1 attenuates renal ischemia-reperfusion injury by improving mitochondrial homeostasis.Journal of cellular and molecular medicine · 2023Article
- miR-22 alleviates sepsis-induced acute kidney injury via targeting the HMGB1/TLR4/NF-κB signaling pathway.International urology and nephrology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Salusin-β is abundantly expressed in many organs and tissues including heart, blood vessels, brain and kidneys. Recent studies have identified salusin-β as a bioactive peptide that contributes to various diseases, such as atherosclerosis, hypertension, diabetes and metabolic syndrome. However, the role of salusin-β in the pathogenesis of acute kidney injury (AKI) is largely unclear. In the present study, we investigated the roles of salusin-β in cisplatin or lipopolysaccharide (LPS)-induced renal injury. Herein, we found that salusin-β expression was upregulated in both renal tubular cells and kidney tissues induced by both cisplatin and LPS. In vitro, silencing of salusin-β diminished, whereas overexpression of salusin-β exaggerated the increased PKC phosphorylation, oxidative stress, histone γH2AX expression, p53 activation and apoptosis in either cisplatin or LPS-challenged renal tubular cells. More importantly, salusin-β overexpression-induced tubular cell apoptosis were abolished by using the PKC inhibitor Go 6976, reactive oxygen species (ROS) scavenger NAC, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor apocynin (Apo) or p53 inhibitor Pifithrin-α. In animals, blockade of salusin-β alleviated PKC phosphorylation, ROS accumulation, DNA damage, and p53 activation as well as renal dysfunction in mice after administration of cisplatin or LPS. Taken together, these results suggest that overexpressed salusin-β is deleterious in AKI by activation of the PKC/ROS signaling pathway, thereby priming renal tubular cells for apoptosis and death.
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