ArticleBMC nephrology2020
RNA-Seq identifies condition-specific biological signatures of ischemia-reperfusion injury in the human kidney.
Article in BMC nephrology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 18 citations in OpenAlex.
- Targeting a Novel AREGCell proliferation · 2026Article
- Research progress of nanoparticles in the diagnosis and treatment of renal ischemia-reperfusion injury.Journal of nanobiotechnology · 2026Review
- Direct scavenging of ROS by S-PPE NP reduces oxidative stress-induced stimulation of the SESN2/AMPK/KIM-1 pathway in acute kidney injury.Renal failure · 2025Article
- Proteomic analysis of human kidney biopsies unveils emerging acute kidney injury very early after liver graft reperfusion.Journal of translational medicine · 2025Article
- PPDPF preserves integrity of proximal tubule by modulating NMNAT activity in chronic kidney diseases.Science advances · 2025Article
- Ischemia-Reperfusion Injury in Kidney Transplantation: Mechanisms and Potential Therapeutic Targets.International journal of molecular sciences · 2024Review
- Acute Kidney Injury by Ischemia/Reperfusion and Extracellular Vesicles.International journal of molecular sciences · 2023Review
- Mitochondrial and NAD+ metabolism predict recovery from acute kidney injury in a diverse mouse population.JCI insight · 2023Article
- Inflammasome pathway in kidney transplantation.Frontiers in medicine · 2023Review
- Comprehensive single-cell transcriptional profiling defines shared and unique epithelial injury responses during kidney fibrosis.Cell metabolism · 2022Article
- Post-Transplant Hypotension in Kidney Recipients-Vasopressin to the Rescue?Kidney international reports · 2022Article
- Fimasartan ameliorates renal ischemia reperfusion injury via modulation of oxidative stress, inflammatory and apoptotic cascades in a rat model.Journal of medicine and life · 2022Article
- Involvement of Inflammasome Components in Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
- The expression of apoptosis related genes in HK-2 cells overexpressingFrontiers in genetics · 2022Article
- Targeting Mitochondria and Metabolism in Acute Kidney Injury.Journal of clinical medicine · 2021Review
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- Delayed Contralateral Nephrectomy Halted Post-Ischemic Renal Fibrosis Progression and Inhibited the Ischemia-Induced Fibromir Upregulation in Mice.Biomedicines · 2021Article
- Network-Based Expression Analyses and Experimental Verifications Reveal the Involvement of STUB1 in Acute Kidney Injury.Frontiers in molecular biosciences · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAcute kidney injury (AKI) is defined as a sudden event of kidney failure or kidney damage within a short period. Ischemia-reperfusion injury (IRI) is a critical factor associated with severe AKI and end-stage kidney disease (ESKD). However, the biological mechanisms underlying ischemia and reperfusion are incompletely understood, owing to the complexity of these pathophysiological processes. We aimed to investigate the key biological pathways individually affected by ischemia and reperfusion at the transcriptome level.
resultsWe analyzed the steady-state gene expression pattern of human kidney tissues from normal (pre-ischemia), ischemia, and reperfusion conditions using RNA-sequencing. Conventional differential expression and self-organizing map (SOM) clustering analyses followed by pathway analysis were performed. Differential expression analysis revealed the metabolic pathways dysregulated in ischemia. Cellular assembly, development and migration, and immune response-related pathways were dysregulated in reperfusion. SOM clustering analysis highlighted the ischemia-mediated significant dysregulation in metabolism, apoptosis, and fibrosis-related pathways, while cell growth, migration, and immune response-related pathways were highly dysregulated by reperfusion after ischemia. The expression of pro-apoptotic genes and death receptors was downregulated during ischemia, indicating the existence of a protective mechanism against ischemic injury. Reperfusion induced alterations in the expression of the genes associated with immune response such as inflammasome and antigen representing genes. Further, the genes related to cell growth and migration, such as AKT, KRAS, and those related to Rho signaling, were downregulated, suggestive of injury responses during reperfusion. Semaphorin 4D and plexin B1 levels were also downregulated.
conclusionsWe show that specific biological pathways were distinctively involved in ischemia and reperfusion during IRI, indicating that condition-specific therapeutic strategies may be imperative to prevent severe kidney damage after IRI in the clinical setting.
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