Evidence map›Paper›PMID 33754657›Full record

ArticleTurkish journal of medical sciences2021

Investigation of the effect of hyperthyroidism on endoplasmic reticulum stress and tran- sient receptor potential canonical 1 channel in the kidney

Nuriye Ezgi Bektur Aykanat, Erhan Şahin, Sedat Kaçar, Rıdvan Bağcı, Şerife Karakaya, Dilek Burukoğlu Dönmez, Varol Şahintürk

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Article in Turkish journal of medical sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 45% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 4 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Nuriye Ezgi Bektur AykanatDepartment of Histology and Embryology, Faculty of Medicine, Atılım University, Ankara, TurkeyORCID 0000-0003-1453-7311
Erhan ŞahinDepartment of Histology and Embryology, Faculty of Medicine, Osmangazi University, Ankara, TurkeyORCID 0000-0003-2152-0542
Sedat KaçarDepartment of Histology and Embryology, Faculty of Medicine, Osmangazi University, Ankara, TurkeyORCID 0000-0002-0671-8529
Rıdvan BağcıDepartment of IVF Unit Andrology Laboratory, Adana City Education and Research Hospital, Adana, TurkeyORCID 0000-0003-0939-1733
Şerife KarakayaDepartment of Histology and Embryology, Faculty of Medicine, Osmangazi University, Ankara, TurkeyORCID 000-0001-9733-0337
Dilek Burukoğlu DönmezDepartment of Histology and Embryology, Faculty of Medicine, Osmangazi University, Ankara, TurkeyORCID 0000-0002-6454-4424
Varol ŞahintürkDepartment of Histology and Embryology, Faculty of Medicine, Osmangazi University, Ankara, TurkeyORCID 0000-0003-2317-3644
Gazi University · TRAtilim University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background/aim: Hyperthyroidism is associated with results in increased glomerular filtration rate as well as increased renin-angio- tensin-aldosterone activation. The disturbance of Ca2+ homeostasis in the endoplasmic reticulum (ER) is associated with many diseases, including diabetic nephropathy and hyperthyroidism. Transient receptor potential canonical 1 (TRPC1) channel is the first cloned TRPC family protein. Although it is expressed in many places in the kidney, its function is uncertain. TRPC1 is involved in regulating Ca2+ homeostasis, and its upregulation increases ER Ca2+ level, activates the unfolded protein response, which leads to cellular damage in the kidney. This study investigated the role of TRPC1 in the kidneys of hyperthyroid rats in terms of ER stress markers that are gluco- se-regulated protein 78 (GRP78), activating transcription factor 6 (ATF6), (protein kinase R (PKR)-like endoplasmic reticulum kinase) (PERK), Inositol-requiring enzyme 1 (IRE1). Materials and methods: Twenty male rats were assigned into control and hyperthyroid groups (n = 10). Hyperthyroidism was induced by adding 12 mg/L thyroxine into the drinking water of rats for 4 weeks. The serum-free T3 and T4 (fT3, fT4), TSH, blood urea nitrogen (BUN), and creatinine levels were measured. The histochemical analysis of kidney sections for morphological changes and also im- munohistochemical and western blot analysis of kidney sections were performed for GRP78, ATF6, PERK, IRE1, TRPC1 antibodies. Results: TSH, BUN, and creatinine levels decreased while fT3 and fT4 levels increased in the hyperthyroid rat. The morphologic analy- sis resulted in the capillary basal membrane thickening in glomeruli and also western blot, and immunohistochemical results showed an increase in TRPC1, GRP78, and ATF6 in the hyperthyroid rat (p < 0.05). Conclusion: In conclusion, in our study, we showed for the first time that the relationship between ER stress and TRPC1, and their increased expression caused renal damage in hyperthyroid rats.

Indexed as

Endoplasmic Reticulum StressHyperthyroidismAnimalsApoptosisCalciumCreatinineKidneyMaleProtein Serine-Threonine KinasesRatsThyrotropinCalciumCreatinineProtein Serine-Threonine KinasesThyrotropinendoplasmic reticulum (ER) stressHyperthyroidismkidneyrattransient receptor potential canonical 1 (TRPC1)

Identifiers

PMID33754657
PMCPMC8283502
OpenAlexW3136455321

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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.