Inflammation and Oxidative Stress in Kidney Disease 2.0
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".
Deadline for manuscript submissions: closed (31 January 2021) | Viewed by 4190
Special Issue Editor
Interests: triple negative breast cancer (TNBC); modulated-electrohyperthermia (mEHT); ischemia induced acute kidney injury (IRI-AKI); non-coding RNAs (miRNA, siRNA, lncRNA); the role of fibrinogen in cell stress
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Special Issue Information
Dear colleagues,
Ischemia-reperfusion injury (IRI) is the leading cause of acute kidney injury (AKI). IRI can lead to renal transplantation as well as circulatory and septic shock. Moreover, it contributes to contrast-induced nephropathy and can lead to chronic kidney disease in the long term. The initial injury is aggravated by subsequent inflammation due to the deliberation of danger-associated molecular patterns (DAMP) and their recognition via toll-like receptors (TLRs). TLRs activate the inflammasome, the interferon (IFN) response, and the subsequent cytokine release initiates inflammation associated with oxidative stress. Cell death is primarily necrotic during ischemia, but tissue damage due to necroptosis or apoptosis occurs during reperfusion. Bacterial endotoxin (lipopolysaccharide)-induced immune-paralysis can provide protection from an otherwise lethal ischemic injury; however, the molecular mechanisms of this cross-tolerance are largely unknown.
An increasing body of evidence suggests that these processes are regulated or modulated by non-coding RNAs (lncRNA, miRNA) and thus can be therapeutically influenced by RNA-based therapies (mRNA, siRNA, ASO). The role of miR-21 has been already well established in disease states, but influencing miR-21 expression did not provide the expected clinical benefit. New miRs and lncRNAs are emerging as potential therapeutic tools to reduce reperfusion injury and chronic kidney disease.
Dr. Peter Hamar
Guest Editor
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