ArticleHistology and histopathology2021
The role and mechanism of PKM2 in the development of LPS-induced acute kidney injury.
Article in Histology and histopathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 12 citations in OpenAlex.
- Biomarkers for Early Detection of Diabetic Kidney Disease in Pediatric and Adolescent Populations: A Narrative Review.Health science reports · 2026Review
- Identification and functional analysis of energy metabolism and pyroptosis-related genes in diabetic nephropathy.Heliyon · 2025Article
- Urinary PKM2, a marker predicating acute kidney injury in patients with sepsis.International urology and nephrology · 2024Article
- Identification of relevant differential genes to the divergent development of pectoral muscle in ducks by transcriptomic analysis.Animal bioscience · 2024Article
- Targeting pyruvate kinase M2 for the treatment of kidney disease.Frontiers in pharmacology · 2024Review
- The role of inflammatory response and metabolic reprogramming in sepsis-associated acute kidney injury: mechanistic insights and therapeutic potential.Frontiers in immunology · 2024Review
- Advances in metabolic reprogramming of renal tubular epithelial cells in sepsis-associated acute kidney injury.Frontiers in physiology · 2024Review
- Pyruvate kinase M2 regulates mitochondrial homeostasis in cisplatin-induced acute kidney injury.Cell death & disease · 2023Article
- Shikonin Alleviates Gentamicin-Induced Renal Injury in Rats by Targeting Renal Endocytosis, SIRT1/Nrf2/HO-1, TLR-4/NF-κB/MAPK, and PI3K/Akt Cascades.Antibiotics (Basel, Switzerland) · 2023Article
- Pyruvate Kinase M2: A New Biomarker for the Early Detection of Diabetes-Induced Nephropathy.International journal of molecular sciences · 2023Article
- Energy metabolic reprogramming regulates programmed cell death of renal tubular epithelial cells and might serve as a new therapeutic target for acute kidney injury.Frontiers in cell and developmental biology · 2023Review
- Proficient Novel Biomarkers Guide Early Detection of Acute Kidney Injury: A Review.Diseases (Basel, Switzerland) · 2022Review
- Podocyte specific deletion of PKM2 ameliorates LPS-induced podocyte injury through beta-catenin.Cell communication and signaling : CCS · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A previous study suggested that pyruvate kinase M2 (PKM2) plays a vital role of metabolic reprogramming in the regulation of the innate inflammatory response, while PKM2 is a sensitive biomarker for nephrotoxicity. In this study, we investigated the role and mechanism of PKM2 in development of LPS-induced acute kidney injury. The AKI model of mice was established using LPS. The serum levels of blood urea nitrogen (Bun), creatinine (Cr), and Cystatin C (CysC) were identified using the enzyme-linked immunosorbent assay (ELISA). Hematoxylin and Eosin staining (H&E) was employed to assess pathological changes in kidney tissues of LPS-induced AKI model. Immunohistochemical staining and Western blot analysis were carried out to determine the expression of apoptosis-related factors at protein levels. We found that Bun, CysC, and Cr were significantly increased in the LPS group compared with the control group. The histopathological assay showed model swollen tubular epithelial cells and the presence of vacuolar degeneration in the LPS-induced AKI. In addition, expression levels of PKM2 significantly increased in the LPS group compared with the control group at both protein and mRNA levels (P<0.01). The inhibition of PKM2 by shikonin notably suppressed the expression of HIF-1α and apoptosis-related factors such as BNIP3, Bax, and Caspase-3, while the inhibition of PKM2 by shikonin significantly improved the histopathological symptoms of LPS-induced AKI. This study demonstrated the potential role of PKM2 in LPS-induced AKI and identified PKM2 as a promising therapeutic target in the treatment of AKI.
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