ArticleFrontiers in pharmacology2021
Acute Kidney Injury is Aggravated in Aged Mice by the Exacerbation of Proinflammatory Processes.
Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 36 citations in OpenAlex.
- Apelin-13 Pretreatment Attenuates Age-Associated Renal Fibrotic Remodeling Following I/R Injury.Biomedicines · 2026Article
- Mitochondrial Dysfunction at the Crossroads of Necroptosis: Mechanisms, Molecular Mediators, and Therapeutic Opportunities.Journal of cellular and molecular medicine · 2026Review
- Dual Roles and Therapeutic Prospects of Proximal Tubular Epithelial Cell Senescence in Acute Kidney Injury.Biomolecules · 2026Review
- Renoprotection by 5-Methoxytryptophan in Kidney Disease.Biomolecules · 2026Review
- Discovery Pipeline for Acute Kidney Injury: Molecules, Mechanisms, Models, and Targets.Nephron · 2026Review
- Remdesivir nephrotoxicity in tubular epithelial cells.Frontiers in pharmacology · 2026Article
- Visnagin Protects Against Lipopolysaccharide-Induced Acute Kidney Injury by Inhibiting Oxidative Stress and Reducing Ferroptosis.International journal of medical sciences · 2026Article
- AI-guided design and optimization of a novel KIM-1-targeted peptide for bFGF delivery in acute kidney injury repair.Regenerative biomaterials · 2026Article
- Haematopoietic ageing in health and lifespan.Nature cell biology · 2025Review
- Cellular senescence in renal ischemia-reperfusion injury.Chinese medical journal · 2025Review
- Dasatinib and Quercetin Combination Increased Kidney Damage in Acute Folic Acid-Induced Experimental Nephropathy.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Protective Effects of a ProbioticFoods (Basel, Switzerland) · 2025Article
- CCN2 Activates Cellular Senescence Leading to Kidney Fibrosis in Folic Acid-Induced Experimental Nephropathy.International journal of molecular sciences · 2025Article
- Update of cellular senescence in kidney fibrosis: from mechanism to potential interventions.Frontiers of medicine · 2025Review
- Understanding COVID-19-related Acute Renal Injury in Elderly Individuals: Preexisting Systemic Inflammation before COVID-19 (SIC).Endocrine, metabolic & immune disorders drug targets · 2025Article
- The mutualistic relationship between M2c macrophages of TGFβ1 induction and gastric cancer cells: the correlation between protective mechanisms in the tumor microenvironment and polarization of subtypes of cells.Journal of Cancer · 2025Article
- A global view of altered ligand-receptor interactions in bone marrow aging based on single-cell sequencing.Computational and structural biotechnology journal · 2024Article
- Article
- Interaction of Fabry Disease and Diabetes Mellitus: Suboptimal Recruitment of Kidney Protective Factors.International journal of molecular sciences · 2023Article
- Elevation of Arginase-II in Podocytes Contributes to Age-Associated Albuminuria in Male Mice.International journal of molecular sciences · 2023Article
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is more frequent in elderly patients. Mechanisms contributing to AKI (tubular cell death, inflammatory cell infiltration, impaired mitochondrial function, and prolonged cell-cycle arrest) have been linked to cellular senescence, a process implicated in regeneration failure and progression to fibrosis. However, the molecular and pathological basis of the age-related increase in AKI incidence is not completely understood. To explore these mechanisms, experimental AKI was induced by folic acid (FA) administration in young (3-months-old) and old (1-year-old) mice, and kidneys were evaluated in the early phase of AKI, at 48 h. Tubular damage score, KIM-1 expression, the recruitment of infiltrating immune cells (mainly neutrophils and macrophages) and proinflammatory gene expression were higher in AKI kidneys of old than of young mice. Tubular cell death in FA-AKI involves several pathways, such as regulated necrosis and apoptosis. Ferroptosis and necroptosis cell-death pathways were upregulated in old AKI kidneys. In contrast, caspase-3 activation was only found in young but not in old mice. Moreover, the antiapoptotic factor BCL-xL was significantly overexpressed in old, injured kidneys, suggesting an age-related apoptosis suppression. AKI kidneys displayed evidence of cellular senescence, such as increased levels of cyclin dependent kinase inhibitors p16ink4a and p21cip1, and of the DNA damage response marker γH2AX. Furthermore, p21cip1 mRNA expression and nuclear staining for p21cip1 and γH2AX were higher in old than in young FA-AKI mice, as well as the expression of senescence-associated secretory phenotype (SASP) components (
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.