Heat shock proteins and kidney disease: perspectives of HSP therapy

Chebotareva, Natalia; Bobkova, Irina; Shilov, E M

doi:10.1007/s12192-017-0790-0

Cited by 83 publications

(83 citation statements)

References 216 publications

(272 reference statements)

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“…Further, many heat shock proteins (HSP) families and their bioactivity are described in various kidney diseases. In ischemic, toxic or other forms of AKI, the following have been found expressed in several renal cell types (podocytes, mesangial cells, tubular cells, fibroblasts, endothelial cells, macrophages): HSP27, HSP70, HSP60, HSP47, HSP90 and HSP32 [ 19 ]. Their main role in renal cytoprotection is still under investigation.…”

Section: Biomarkers Of Sepsis-induced Acute Kidney Injurymentioning

confidence: 99%

Acute Kidney Injury in Septic Patients Treated by Selected Nephrotoxic Antibiotic Agents—Pathophysiology and Biomarkers—A Review

Petejová

Martínek

Zadrazil

et al. 2020

IJMS

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Acute kidney injury is a common complication in critically ill patients with sepsis and/or septic shock. Further, some essential antimicrobial treatment drugs are themselves nephrotoxic. For this reason, timely diagnosis and adequate therapeutic management are paramount. Of potential acute kidney injury (AKI) biomarkers, non-protein-coding RNAs are a subject of ongoing research. This review covers the pathophysiology of vancomycin and gentamicin nephrotoxicity in particular, septic AKI and the microRNAs involved in the pathophysiology of both syndromes. PubMED, UptoDate, MEDLINE and Cochrane databases were searched, using the terms: biomarkers, acute kidney injury, antibiotic nephrotoxicity, sepsis, miRNA and nephrotoxicity. A comprehensive review describing pathophysiology and potential biomarkers of septic and toxic acute kidney injury in septic patients was conducted. In addition, five miRNAs: miR-15a-5p, miR-192-5p, miR-155-5p, miR-486-5p and miR-423-5p specific to septic and toxic acute kidney injury in septic patients, treated by nephrotoxic antibiotic agents (vancomycin and gentamicin) were identified. However, while these are at the stage of clinical testing, preclinical and clinical trials are needed before they can be considered useful biomarkers or therapeutic targets of AKI in the context of antibiotic nephrotoxicity or septic injury.

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Section: Biomarkers Of Sepsis-induced Acute Kidney Injurymentioning

confidence: 99%

Acute Kidney Injury in Septic Patients Treated by Selected Nephrotoxic Antibiotic Agents—Pathophysiology and Biomarkers—A Review

Petejová

Martínek

Zadrazil

et al. 2020

IJMS

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“…However, the assessment of APAP-induced early liver impairment before clinical diagnosis remains uninvestigated. Biologically, production of high level of heat shock protein can be triggered by exposure to different kinds of environmental stress conditions, such as infection, inflammation, toxin induction [9]. Hsp90 is involved in activation of steroid receptor and transcription factor, showing as a promising anti-apoptotic effector [10].…”

Section: Introductionmentioning

confidence: 99%

Biocharacterization of Heat Shock Protein 90 in Acetaminophen-Treated Livers Without Conspicuous Drug Induced Liver Injury

Wu¹,

Guo²,

Su³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Acetaminophen (APAP) refers to a medication used to manage pain and fever symptoms. Heat shock protein 90 (Hsp90) is to be expressed during various stresses, such as wound healing and tissue remodeling. Recently, it is discovered that Hsp90 is a potential modifier of cytogenesis. In comparison to clinical references of liver damage, this study was designed to assess the potential bioeffect of Hsp90 in APAP-treated livers without conspicuous drug induced liver injury (DILI). Methods: In our current study, human plasma samples of APAP-used patients were collected for biochemical assays in clinical parameters. Adult male mice were used to investigate the biocharacterization of Hsp90 in APAP-treated livers through serological tests and immunoassays. Further, a mouse liver cell strain was employed in assessment of bioeffect of APAP on hepatocellular Hsp90 expression. Results: Correspondingly, the clinical data showed APAP-administered patients resulted in increased Hsp90 levels in serum when compared to other clinical parameters of liver injury. In adult mice study, APAP-treated livers showed unchanged hepatocellular and metabolic functions, as highlighted in biochemical analysis and immunoassay. Notably, Hsp90 expression in APAP-treated mice were elevated in the serum and liver samples. In quantitative western blot assay, the present data suggested that hepatocellular Hsp90 level was up-regulated followed by APAP treatment. In mouse cell strain study, APAP-treated liver cells had increased trend of aminotransferase contents and apoptotic counts. Further, endogenous Hsp90 expression in APAP-exposed cells was increased dose- and time-dependently. Conclusions: In conclusion, our current findings disclose that Hsp90 biomolecule may be a potential indicator for APAP-induced inconspicuous DILI, in which it seems to be characterized with more sensitive than other diagnosis criteria.

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“…14 Defects in the function of HSPs could contribute to diabetic complications including nephropathy. 15 Among the many physiological, pharmacological, and genetic approaches that have been postulated to address HSP-targeted therapies in both experimental and clinical setting, 1 physical exercise provides a physiological stimulus of heat shock factor-1 (HSF-1), which translocates to the nucleus upon activation and binds to heat shock elements resulting in increased HSP expression. 16,17 HSPs potentially act in buffering tissues against disease-associated homeostatic disturbance and thereby contribute to the positive biological effects in diabetes.…”

mentioning

confidence: 99%

Suppressed heat shock protein response in the kidney of exercise‐trained diabetic rats

Lappalainen

Oksala

Laaksonen

et al. 2018

Scandinavian Med Sci Sports

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Impaired expression of heat shock proteins (HSPs) and increased oxidative stress may contribute to the pathophysiology of diabetes by disrupted tissue protection. Acute exercise induces oxidative stress, whereas exercise training up-regulates endogenous antioxidant defenses and HSP expression. Although diabetic nephropathy is a major contributor to diabetic morbidity, information regarding the effect of HSPs on kidney protection is limited. This study evaluated the effects of eight-week exercise training on kidney HSP expression and markers of oxidative stress at rest and after acute exercise in rats with or without streptozotocin-induced diabetes. Induction of diabetes increased DNA-binding activity of heat shock factor-1, but decreased the expression of HSP72, HSP60, and HSP90. The inflammatory markers IL-6 and TNF-alpha were increased in the kidney tissue of diabetic animals. Both exercise training and acute exercise increased HSP72 and HSP90 protein levels only in non-diabetic rats. On the other hand, exercise training appeared to reverse the diabetes-induced histological changes together with decreased expression of TGF-beta as a key inducer of glomerulosclerosis, and decreased levels of IL-6 and TNF-alpha. Notably, HSP72 and TGF-beta were negatively correlated. In conclusion, impaired HSP defense seems to contribute to kidney injury vulnerability in diabetes and exercise training does not up-regulate kidney HSP expression despite the improvements in histopathological and inflammatory markers.

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Heat shock proteins and kidney disease: perspectives of HSP therapy

Cited by 83 publications

References 216 publications

Acute Kidney Injury in Septic Patients Treated by Selected Nephrotoxic Antibiotic Agents—Pathophysiology and Biomarkers—A Review

Acute Kidney Injury in Septic Patients Treated by Selected Nephrotoxic Antibiotic Agents—Pathophysiology and Biomarkers—A Review

Biocharacterization of Heat Shock Protein 90 in Acetaminophen-Treated Livers Without Conspicuous Drug Induced Liver Injury

Suppressed heat shock protein response in the kidney of exercise‐trained diabetic rats

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