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Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
Published on: June 7, 2014
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Hyperthyroidism exacerbates ischemic reperfusion injury in the kidney
Yasuno Yamaguchi1, Kohei Uchimura1, Kazuya Takahashi1
1Division of Nephrology, Department of Internal Medicine, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Yamanashi 409-3898, Japan.
Endocrine Journal
|October 11, 2021
Summary
Excess thyroid hormones worsen kidney injury following ischemic stress by increasing cell damage and inflammation. Blocking thyroid hormone receptor beta (TRβ) in kidney cells protected against this damage, suggesting a key role for TRβ in hyperthyroidism-induced kidney problems.
Area of Science:
- Endocrinology
- Nephrology
- Molecular Biology
Background:
- Thyroid hormones regulate metabolism and development.
- Hyperthyroidism, or excess thyroid hormones, activates thyroid hormone receptors (TRs).
- Arginase 2 (ARG2) overexpression, downstream of TRs, increases reactive oxygen species and exacerbates kidney ischemia/reperfusion (I/R) injury.
Purpose of the Study:
- To investigate the association between hyperthyroidism and I/R-induced kidney injury.
- To determine the role of thyroid hormone receptor beta (TRβ) in hyperthyroid kidney injury.
Main Methods:
- Mice were pretreated with L-thyroxine (LT4) to induce hyperthyroidism or vehicle.
- Kidney I/R injury was induced in mice.
- Proximal tubular cell-specific conditional knockout of TRβ (TRβcKO) mice were generated and subjected to I/R.
Main Results:
- Hyperthyroidism exacerbated tubular damage, fibrosis, and necroptosis in kidneys post-I/R.
- Inflammatory cell accumulation, ARG2 expression, and reactive oxygen species increased in hyperthyroid kidneys after I/R.
- TRβcKO mice showed ameliorated kidney injury, reduced ARG2, and decreased reactive oxygen species after I/R compared to control mice.
Conclusions:
- Excess thyroid hormones are detrimental to kidneys under ischemic stress.
- TRβ mediates hyperthyroidism-induced kidney injury.
- Iatrogenic thyrotoxicosis from LT4 overreplacement may cause kidney damage.
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