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Volume 20, Issue 2 (May 2026)
IJT 2026, 20(2): 96-104 |
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Ethics code: Not applicable (Literature-based study)
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Martantiningtyas D C, Puspasari G, Ivone J, Hasianna S T, Imelda I, Larissa L, et al . Microplastics and Renal Ischemia–Reperfusion Injury: Integrative Mechanisms, Co-Contaminant Synergy, and Therapeutic Strategies. IJT 2026; 20 (2) :96-104
URL: http://ijt.arakmu.ac.ir/article-1-1558-en.html
URL: http://ijt.arakmu.ac.ir/article-1-1558-en.html
Demes Chornelia Martantiningtyas *1 
, Grace Puspasari2 , July Ivone3 , Stella Tinia Hasianna4 , Imelda Imelda5 , Larissa Larissa6 , Hartini Hartini5 , Wenny Wati3 , Eti Nurwening Sholikhah7 , Hanggoro Tri Rinonce7
, Grace Puspasari2 , July Ivone3 , Stella Tinia Hasianna4 , Imelda Imelda5 , Larissa Larissa6 , Hartini Hartini5 , Wenny Wati3 , Eti Nurwening Sholikhah7 , Hanggoro Tri Rinonce7
1- Department of Biochemistry, Faculty of Medicine, Maranatha Christian University, Bandung, Indonesia. & PhD Candidate in Biomedical Sciences, Faculty of Medicine, Public Health and Nursing, Universitas Gadjah Mada, Yogyakarta, Indonesia , demes.cm@med.maranatha.edu
2- PhD Candidate in Biomedical Sciences, Faculty of Medicine, Public Health and Nursing, Universitas Gadjah Mada, Yogyakarta, Indonesia
3- Department of Public Health, Faculty of Medicine, Maranatha Christian University, Bandung, Indonesia.
4- Department of Physiology, Faculty of Medicine, Maranatha Christian University, Bandung, Indonesia.
5- Department of Histology, Faculty of Medicine, Maranatha Christian University, Bandung, Indonesia.
6- Department of Anatomical Pathology, Faculty of Medicine, Maranatha Christian University, Bandung, Indonesia.
7- Department of Anatomical Pathology, Faculty of Medicine, Public Health and Nursing, Dr Sardjito Hospital, Universitas Gadjah Mada, Yogyakarta, Indonesia
2- PhD Candidate in Biomedical Sciences, Faculty of Medicine, Public Health and Nursing, Universitas Gadjah Mada, Yogyakarta, Indonesia
3- Department of Public Health, Faculty of Medicine, Maranatha Christian University, Bandung, Indonesia.
4- Department of Physiology, Faculty of Medicine, Maranatha Christian University, Bandung, Indonesia.
5- Department of Histology, Faculty of Medicine, Maranatha Christian University, Bandung, Indonesia.
6- Department of Anatomical Pathology, Faculty of Medicine, Maranatha Christian University, Bandung, Indonesia.
7- Department of Anatomical Pathology, Faculty of Medicine, Public Health and Nursing, Dr Sardjito Hospital, Universitas Gadjah Mada, Yogyakarta, Indonesia
Abstract: (127 Views)
Background: Microplastics (MPs) are increasingly recognized as environmental toxicants capable of accumulating in renal tissue. Experimental studies suggest that MPs may aggravate renal ischemia–reperfusion injury (IRI); however, the strength of evidence varies, and mechanistic conclusions often rely on indirect data.
Methods: This narrative review synthesized experimental evidence on microplastic-induced renal toxicity and renal ischemia-reperfusion injury, with emphasis on oxidative stress, inflammation, mitochondrial dysfunction, endothelial injury, and related mechanistic pathways.
Results: Direct evidence from rodent IRI models indicates that prior MP exposure worsens tubular damage, increases oxidative stress markers, and enhances inflammatory activation during reperfusion. These findings support a contributory role for MPs in amplifying reactive oxygen species (ROS) generation, mitochondrial dysfunction, and downstream inflammatory pathways during IRI. In contrast, additional mechanisms frequently discussed in MP nephrotoxicity—such as ferroptosis, endothelial remodelling, epigenetic alterations, and co-contaminant–mediated toxicity—are largely based on non-ischemic kidney models or extra-renal systems. Distinguishing mechanistic pathways supported by direct evidence from those that remain hypothetical is essential for clarifying how MPs may influence IRI severity.
Conclusion: Current literature indicates that MPs exacerbate renal IRI primarily through oxidative and inflammatory mechanisms, while other pathways remain plausible but unproven. Further research using dedicated MP–IRI models is needed to validate these mechanisms and guide targeted therapeutic interventions.
Methods: This narrative review synthesized experimental evidence on microplastic-induced renal toxicity and renal ischemia-reperfusion injury, with emphasis on oxidative stress, inflammation, mitochondrial dysfunction, endothelial injury, and related mechanistic pathways.
Results: Direct evidence from rodent IRI models indicates that prior MP exposure worsens tubular damage, increases oxidative stress markers, and enhances inflammatory activation during reperfusion. These findings support a contributory role for MPs in amplifying reactive oxygen species (ROS) generation, mitochondrial dysfunction, and downstream inflammatory pathways during IRI. In contrast, additional mechanisms frequently discussed in MP nephrotoxicity—such as ferroptosis, endothelial remodelling, epigenetic alterations, and co-contaminant–mediated toxicity—are largely based on non-ischemic kidney models or extra-renal systems. Distinguishing mechanistic pathways supported by direct evidence from those that remain hypothetical is essential for clarifying how MPs may influence IRI severity.
Conclusion: Current literature indicates that MPs exacerbate renal IRI primarily through oxidative and inflammatory mechanisms, while other pathways remain plausible but unproven. Further research using dedicated MP–IRI models is needed to validate these mechanisms and guide targeted therapeutic interventions.
Keywords: Inflammation, Kidney toxicity, Microplastics, Oxidative stress, Renal ischemia–reperfusion injury
Type of Study: Applicable |
Subject:
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The Iranian Journal of Toxicology
Arak University of Medical Sciences in collaboration with the Iranian Society of Toxicology
Website: http://ijt.arakmu.ac.ir
Email: tox.journal@gmail.com
