The DOI matches its Crossref record; 73 of the 74 references it cites were found in a registry or an index.
IL-6 promotes nonthyroidal illness syndrome by blocking thyroxine activation while promoting thyroid hormone inactivation in human cells
Open accessAbstract
Nonthyroidal illness syndrome (NTIS) is a state of low serum 3,5,3' triiodothyronine (T₃) that occurs in chronically ill patients; the degree of reduction in T₃ is associated with overall prognosis and survival. Iodthyronine deiodinases are enzymes that catalyze iodine removal from thyroid hormones; type I and II deiodinase (D1 and D2, respectively) convert the prohormone thyroxine T₄ to active T₃, whereas the type III enzyme (D3) inactivates T₄ and T₃. Increased production of cytokines, including IL-6, is a hallmark of the acute phase of NTIS, but the role of cytokines in altered thyroid hormone metabolism is poorly understood. Here, we measured the effect of IL-6 on both endogenous cofactor-mediated and dithiothreitol-stimulated (DTT-stimulated) cell sonicate deiodinase activities in human cell lines. Active T₃ generation by D1 and D2 in intact cells was suppressed by IL-6, despite an increase in sonicate deiodinases (and mRNAs). N-acetyl-cysteine (NAC), an antioxidant that restores intracellular glutathione (GSH) concentrations, prevented the IL-6-induced inhibitory effect on D1- and D2-mediated T₃ production, which suggests that IL-6 might function by depleting an intracellular thiol cofactor, perhaps GSH. In contrast, IL-6 stimulated endogenous D3-mediated inactivation of T₃. Taken together, these results identify a single pathway by which IL-6-induced oxidative stress can reduce D1- and D2-mediated T₄-to-T₃ conversion as well as increasing D3-mediated T₃ (and T₄) inactivation, thus mimicking events during illness.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In addition, decreased availability of glutathione (GSH), a co-factor required for DIO1 catalytic activity, may also play a role [80].”
From An update on non-thyroidal illness syndrome (2021) · cites this paper as [80]
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Free radicals and antioxidants in normal physiological functions and human disease
Valko, M., Leibfritz, D., Moncol, J., Cronin, M. T. D., Mazur, M., & Telser, J. (2007) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2006.07.001 · Cited by 14,269
Meister, A., & Anderson, M. E. (1983) · Annual Review of Biochemistry · doi:10.1146/annurev.bi.52.070183.003431 · Cited by 5,694
Schafer, F. Q., & Buettner, G. R. (2001) · Free Radical Biology and Medicine · doi:10.1016/s0891-5849(01)00480-4 · Cited by 4,587
Williams Textbook of Endocrinology
Melmed, S., & Polonsky, K. S. (2016) · Elsevier eBooks · doi:10.1016/c2013-0-15980-6 · Cited by 3,715
Meier, B., Radeke, H. H., Selle, S., Younes, M., Sies, H., Resch, K., & Habermehl, G. (1989) · Biochemical Journal · doi:10.1042/bj2630539 · Cited by 650
Lu, J., & Holmgren, A. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.r800045200 · Cited by 618
Low-T3 syndrome: a strong prognostic predictor of death in patients with heart disease
Iervasi, G., Pingitore, A., Landi, P., Raciti, M., Ripoli, A., Scarlattini, M., L’Abbate, A., & Donato, L. (2003) · Circulation · doi:10.1161/01.cir.0000048124.64204.3f · Cited by 472
Peeters, R. P., Wouters, P. J., Kaptein, E., van Toor, H., Visser, T. J., & Van den Berghe, G. (2003) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2002-022013 · Cited by 452
Euthyroid Sick Syndrome: Is It a Misnomer?
Chopra, I. J. (1997) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.82.2.3745 · Cited by 374
Type 2 iodothyronine deiodinase is the major source of plasma T3 in euthyroid humans
Luiza Maia, A. (2005) · Journal of Clinical Investigation · doi:10.1172/jci25083 · Cited by 360
Flagged first, then by citations
1 of the 74 references couldn’t be matched to a known paper.
Research works printed but not linked: 8
- 10.1210/jc.82.2.329 · DOI · Paper page
- 10.1210/jc.77.6.1695 · DOI · Paper page
- 10.1210/en.141.11.4309 · DOI
- 10.1210/en.143.4.1190 · DOI
- 10.1210/en.141.3.1127 · DOI · Paper page
- 10.1210/me.14.11.1697 · DOI · Paper page
- 10.1210/en.133.4.1715 · DOI
- 10.1210/en.134.6.2490 · DOI
Cited by
Sorted by citations
Items 101–167 of 167
Xu, M., Liu, G., Cao, L., Bai, X.-F., Kang, L., Zhao, X., Shi, X.-N., & Li, L. (2020) · PubMed Central · doi:10.7499/j.issn.1008-8830.2004137 · Cited by 5
“NTIS 的 诊 断 标 准：（1） 临 床 上 各 种 引 起 NTIS 的基础疾病；（2）无明显甲状腺疾病的存在； （3） 有甲状腺激素和促甲状腺激素的特定变化 [11]。 NTIS 可分为 3 型。低 T3 型：血清 T3 降低， T4 正常或升高；低 T3 低 T4 型：血清 T3、T4 均 降低；高 T4 型：血清 T4 升高 [11]。 所有研究对象在入院 24 h 内采集晨起空腹 静脉血行甲状腺功能测定。血样以 3 000 r/min 离 心 15 min，分离血清，于 -20℃冰箱保存。使用 Beckman Access 分析仪进行化学发光免疫分析，测 定血清 T3、T4、游离三碘酪氨酸（fT3）、游离四 碘酪氨酸…”
BackgroundInfluentialWang, G., Gao, T., Liu, Y., Duan, J., Lu, H., Jiang, A., Xu, Y., Lu, X., Li, X., Wang, Y., et al. (2024) · Burns & Trauma · doi:10.1093/burnst/tkae066 · Cited by 5
Induction of type 2 and 3 deiodinase in the blood cells of critically ill patients
Oliveira, T. C., Braun, A. C., Dutra, R. P. D., Breit, M. M. M., Abib, J. B., Thomazini, L. D., Argenti, G., Correa, M. P. A., Almeida, G., Vidart, J., et al. (2025) · Endocrine Connections · doi:10.1530/ec-24-0677 · Cited by 4
“D3 is crucial in neutrophil function, including migration and intracellular killing capabilities (17, 18).”
Self-citationBiletska, O. M., Latohuz, S. I., & Garyachiy, Y. V. (2025) · Experimental and Clinical Medicine · doi:10.35339/ekm.2025.94.3.blg · Cited by 6
Evaluation of thyroid function abnormalities in sixty dogs naturally infected with Babesia canis
Kučer, N., Marin, H. P., Gotić, J., Kuleš, J., Tršan, J., Kajin, F., & Rafaj, R. B. (2019) · Veterinarski arhiv · doi:10.24099/vet.arhiv.0543 · Cited by 4
“In research on human cells it was found that IL-6 reduces conversion of T4 to T3 by reducing the activity of D1 and D2 deiodinases, and increases D3 deiodinase activity, consequently causing increased inactivation of the thyroid hormone (WAJNER et al., 2011).”
BackgroundCytokines in Endocrine Dysfunction of Plasma Cell Disorders
Feigerlová, E., & Battaglia-Hsu, S.-F. (2017) · Mediators of Inflammation · doi:10.1155/2017/7586174 · Cited by 4
“Mechanistically, IL-6 suppresses D1- (type I deiodinase-) and D2- (type II deiodinase-) mediated T4-to-T3 conversion and increases D3- (type III deiodinase-) mediated T3 (and T4) inactivation via the MAPK pathway [69] (Figure 2).”
BackgroundInfluentialThe endocrinology of thyroid disease from 2005 to 2015
Larsen, P. R. (2015) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2015.169 · Cited by 4
Self-citationImpact of Thyroid Disease on Heart Failure
Stanciu, A. E., Zamfir‐Chiru‐Anton, A., Stanciu, M., & Gheorghe, D. C. (2017) · InTech eBooks · doi:10.5772/66283 · Cited by 4
“Also, it is known that IL‐6 is a hallmark of the acute phase of low T3 syndrome [21].”
BackgroundKovačević, M., Nesek-Adam, V., Klokić, S., & Mujarić, E. (2024) · World Journal of Critical Care Medicine · doi:10.5492/wjccm.v13.i3.96132 · Cited by 4
Odriozola-Martínez, A., González, A., Odriozola, I., Corbi, F., & Álvarez‐Herms, J. (2025) · Nutrients · doi:10.3390/nu18010059 · Cited by 3
“In the context of endurance training, these combined disturbances may manifest as slower recovery, reduced thermogenesis, and fatigue, features that conceptually re-semble an energy-conservation phenotype within the broader model of maladaptive thyroid–microbiota interaction [20,118].”
Wu, Y., Zhou, H., Ci, X., & Lu, J. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2024.1357633 · Cited by 3
“Another plausible explanation for low T3 syndrome involves the regulatory effect of IL-6 on TH, with IL-6 reported to inhibit TH activation while promoting its inactivation in human cells ( Wajner et al., 2011).”
BackgroundZhu, B., Shrivastava, A., Luongo, C., Chen, T., Harney, J. W., Marsili, A., Tran, T.-V., Bhadouria, A., Mopala, R., Steen, A. I., et al. (2012) · Journal of Endocrinology · doi:10.1530/joe-11-0459 · Cited by 3
“…suggested that exposure to saturating substrate concentrations oxidizes the D1 enzyme, although it is puzzling as to why the D1 enzyme cannot be adequately regenerated by endogenous co-factors within the cell (St Germain 1988b, St Germain & Croteau 1989, Croteau et al. 1998, Wajner et al. 2011).”
Self-citationNorris, B. M., Chorbajian, A., Dawi, J., Mohan, A. S., Glassman, I., Ochsner, J., Misakyan, Y., Abnousian, A., Kiriaki, A., Sasaninia, K., et al. (2024) · Antioxidants · doi:10.3390/antiox13030271 · Cited by 3
“The SARS-CoV-2 viral N protein has been found to increase the synthesis of IL-6, which has been linked to the downregulation of glutamate cysteine ligase (GCL), the rate-limiting enzyme in GSH synthesis [12,13].”
BackgroundOliveira, T. S., Shimabukuro, M. K., Monteiro, V. R. D. S., de Andrade, C. B. V., Boelen, A., Wajner, S. M., Maia, A. L., Ortiga-Carvalho, T. M., & Bloise, F. F. (2022) · Metabolites · doi:10.3390/metabo12050416 · Cited by 5
“D2 activity was measured as previously described [40].”
MethodSelf-citationTissue-Specific Regulation of Thyroid Status by Selenodeiodinases
Marsili, A., Larsen, P. R., & Zavacki, A. M. (2016) · Springer eBooks · doi:10.1007/978-3-319-41283-2_41 · Cited by 3
Self-citationEuthyroid Sick Syndrome as an Index of Prognosis in Severe COVID-19 Disease
Athanassiou, L., Kostoglou‐Athanassiou, I., Kaiafa, G. D., Nikolakopoulou, S., Konstantinou, A., Mascha, O., Samaras, C., Savopoulos, C., Shoenfeld, Y., & Athanassiou, P. (2025) · Medicina · doi:10.3390/medicina61081372 · Cited by 2
Endocrine disruptions in thermal injuries: exploring immune system interactions
Khalaf, F., Wojtowicz‐Piotrowski, S., Ricciuti, Z., Dadashizadeh, G., Barayan, D., & Jeschke, M. G. (2026) · Physiological Reviews · doi:10.1152/physrev.00035.2025 · Cited by 2
Zhang, X., Tripathi, M., Goh, C. T., Chan, C. S., Boelen, A., Yen, P. M., Singh, B. K., & Bruinstroop, E. (2026) · Aging Cell · doi:10.1111/acel.70600 · Cited by 2
“This association could be caused by cytokines such as IL-6 and IL-1β , known SASP components, which have been shown to reduce Dio1 activity and induce Dio3 expression (Bruinstroop et al. 2023; Wajner et al. 2011).”
Meng, X., Lv, A., Tang, M., Liu, X., Wang, X., Li, Y., Chai, Y., Yang, Q., Kou, C., Zhang, L., et al. (2024) · Clinical Rheumatology · doi:10.1007/s10067-024-06947-y · Cited by 2
“The activation of cytokines leads to a decrease in ORD activity by mediating an imbalance in deio-dinase activity, primarily through a reduction in ID1 mRNA expression and activity in the hepatic system [12].”
Akman, B. T., Topaloğlu, O., Altunoğlu, A., Neşeli̇oğlu, S., & Erel, Ö. (2021) · Postgraduate Medicine · doi:10.1080/00325481.2021.1994267 · Cited by 2
“Euthyroid sick syndrome (ESS), in other terms low T3 syndrome or nonthyroidal illness syndrome, is supposed to be a disease associated with OS [7,8] and the release of inflammatory cytokines such as Interleukin-6 (IL-6) [9,10].”
InfluentialArticle Review: Immunological Markers Related with Thyroidisum
Hamadi, G. M. (2022) · International Journal for Research in Applied Sciences and Biotechnology · doi:10.31033/ijrasb.9.2.4 · Cited by 1
“Inside a subsequent Reaction mixture, all pathologic alterations revealed validated utilizing Platinum Taq High-Fidelity DNA Polymerase (Invitrogen) underneath the identical circumstances as before([71]).”
MethodAre Changes in Thyroid Hormones Associated with Mortality in Non-Thyroidal Illness Syndrome?
Hoca, E., Ataoğlu, H. E., & Ahbab, S. (2021) · European Journal of Clinical Medicine · doi:10.24018/clinicmed.2021.2.6.148 · Cited by 1
Dysregulation of hepatic deiodinase type I in metabolically associated steatotic liver disease
López‐Alcántara, N., Naujack, A.-M., Chen, Y., Taege, N., Geißler, C., Oelkrug, R., Wirth, E. K., Schomburg, L., Boelen, A., Kirchner, H., et al. (2025) · Journal of Molecular Endocrinology · doi:10.1530/jme-25-0096 · Cited by 1
Elliott, J., Kamaleldeen, E. B., Davis, P., Dias, R. P., Boelaert, K., & Mohamed, Z. (2025) · JCEM Case Reports · doi:10.1210/jcemcr/luaf309 · Cited by 1
Fujisawa, C., Fujisawa, H., Matsui, Y., Sugimoto, T., Minakami, M., Watanabe, K., Yamada, Y., Nakashima, H., Komiya, H., Sugimura, Y., et al. (2026) · Journal of Alzheimer s Disease · doi:10.1177/13872877261424207 · Cited by 1
“50 Another factor may be selenium de fi ciency or impaired selenium utilization, because deiodinase activity requires the selenocysteine residue.”
Современные представления о синдроме эутиреоиднои патологии в клинической практике
Abramova, N., & Pashkovska, N. V. (2017) · Likarska sprava · doi:10.31640/ls-2017(1-2)04 · Cited by 1
Ouyang, H., Huang, M., Chen, S., Wu, X., & Zhou, D. (2022) · Psychiatry Research · doi:10.1016/j.psychres.2022.114546 · Cited by 1
Bender, J. G., Ribeiro, R. T., Zemniaçak, Â. B., Palavro, R., Marschner, R. A., Wajner, S. M., Castro, E. T., Leipnitz, G., Wajner, M., & Amaral, A. U. (2024) · Cell Biochemistry and Function · doi:10.1002/cbf.70010 · Cited by 1
Self-citationYang, S., Liao, K., Zhou, L., Zhang, S., & Wu, J.-C. (2025) · Frontiers in Nutrition · doi:10.3389/fnut.2025.1539022 · Cited by 1
TH Metabolism in Ischemia/Reperfusion Models
Kusmic, C., & L’Abbate, S. (2020) · Springer eBooks · doi:10.1007/978-3-030-36871-5_6 · Cited by 1
Παππά, Θ., & Alevizaki, M. K. (2017) · Endocrinology · doi:10.1007/978-3-319-29195-6_26-1 · Cited by 1
Marschner, R. A., Roginski, A. C., Ribeiro, R. T., Longo, L., de Freitas, L. B. R., Álvares‐da‐Silva, M. R., & Wajner, S. M. (2022) · Preprints.org · doi:10.20944/preprints202212.0091.v1 · Cited by 1
Self-citationN-Acetylcysteine Prevents the Decrease of Serum T 3 in Patients with Acute Myocardial Infarction
Burger, A. (2014) · Clinical Thyroidology · doi:10.1089/ct.2014;26.297-299
How to Make a Thyroid Hypothyroid
Peeters, R. P., & Visser, T. J. (2012) · Thyroid · doi:10.1089/thy.2012.2209.ed
Effect of N-acetylcysteine on serum thyroid hormone levels in nonthyroidal illness syndrome
Vidart, J., Wajner, S. M., Schaan, B. D., & Maia, A. (2013) · Critical Care · doi:10.1186/cc12653
Self-citationThyroid Hormone Metabolism and Transport
Germain, D. L. S., & Hernández, A. (2015) · Elsevier eBooks · doi:10.1016/b978-0-323-18907-1.00076-7 · Cited by 1
The research progress of low T3 syndrome
Hu, Y., & Ye, S. (2015)
Abramova, N., & Pashkovska, N. V. (2017) · Likarska sprava · doi:10.31640/ls-2017(3-4)07
Endocrine Disorders: Integrative Treatments of Hypothyroidism, Diabetes, and Adrenal Dysfunction
Yang, J. (2017) · Oxford University Press eBooks · doi:10.1093/med/9780190466268.003.0014
Baneshi, A. R., Nowroozi-Asl, A., Darya, G. H., Hashemi, F., & Musavi, S. M. (2019) · Iranian South Medical Journal · doi:10.29252/ismj.22.3.141
Endocrine Responses to Critical Illness
Gunst, J., Boonen, E., & den Berghe, G. V. (2018) · Wiley eBooks · doi:10.1002/9781119374800.ch3
薛, 万. (2021) · Advances in Clinical Medicine · doi:10.12677/acm.2021.113127
Leite, A. R., Neves, J. S., Angélico‐Gonçalves, A., Vasques‐Nóvoa, F., Saraiva, F. A., Pinho, I. B., Oliveira, A., Borges‐Canha, M., von Hafe, M., Vale, C., et al. (2022) · Research Square · doi:10.21203/rs.3.rs-2042487/v1
IMPACT OF SARS-CoV-2 INFECTION ON THYROID FUNCTION – PATOMECHANISM AND CLINICAL IMPLICATIONS
Rabiza, A., Słowińska, A., Głuszak, P., Winkel, K., Kurzyca, J., & Owecki, M. (2023) · Postepy Biologii Komorki · doi:10.59674/pbk7
Ullah, M., Hasan, M. M., Khalequzzaman, M., Islam, K. N., Rahman, M. M., & Easmin, T. (2023) · Cardiovascular Journal · doi:10.3329/cardio.v16i1.68206
Marschner, R. A., Oliveira, T. C., Dreher, M. P., Correa, J. M., Ribeiro, R. T., Gayger-Dias, V., Silva, V. F., de Freitas, L. B. R., Gonçalves, C. A., Álvares‐da‐Silva, M. R., et al. (2023) · Research Square · doi:10.21203/rs.3.rs-3304213/v1
Self-citationLiu, Y., Huo, J., Ge, M., Li, X., Huang, J., Ren, X., Wang, M., Nie, N., Zhang, J., Jin, P., et al. (2024) · Blood Science · doi:10.1097/bs9.0000000000000182
“13 TNF-α activates the nuclear factor-κ B (NF-κ B) pathway to inhibit the activity of deiodinase, causing ESS.”
BackgroundPop, V. J. M., Krabbe, J. G., Broeren, M. A. C., Wiersinga, W. M., & Rayman, M. P. (2024) · European Thyroid Journal · doi:10.1530/etj-23-0163
“Second, inflammation (high IL-6) may suppress the deiodination of T4 by deiodinases D1 and D2 eventually resulting in lower TH in tissue (23).”
BackgroundType 3 Deiodinase is Induced in Brain Of Two Models Leading to Cognitive ImpairmentPreprint
Dreher, M. P., Oliveira, T. C., Sindo, J., Solari, M. I. G., Ribeiro, R. T., Longo, L., Gayger-Dias, V., Silva, V.-F. D., de Freitas, L. B. R., Gonçalves, C., et al. (2024) · Research Square · doi:10.21203/rs.3.rs-4222656/v1
Self-citationMaruoka, A., Kimura, A., Hattori, F., Hitomi, H., Osafune, K., Shiojima, I., & Toyoda, N. (2024) · Research Square · doi:10.21203/rs.3.rs-4745956/v1
Ma, Y., Miao, C., Wei, J., Sun, B., Li, H., Tian, Y., & Zhu, Y. (2024) · Chemosphere · doi:10.1016/j.chemosphere.2024.143610
“Also, the activation of thyroxine can be blocked by specific inflammatory factors such as IL-6, which in turn promotes the development of nonthyroidal illness syndrome (Wajner et al., 2011).”
BackgroundAprilia, D., Decroli, E., & Fadella, A. (2025) · Health & Medical Journal · doi:10.33854/heme.v7i1.1639
Maruoka, A., Kimura, A., Hattori, F., Hitomi, H., Osafune, K., Shiojima, I., & Toyoda, N. (2025) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2025.112490
Aimaganova, A., Khovanova, N. A., Braybrook, E., Vryonis, E., Anderson, N. R., Young, L. S., & Grammatopoulos, D. K. (2025) · Scientific Reports · doi:10.1038/s41598-025-25434-1
“…that includes altered hypothalamic ‘set - points’ that initiate thyrotropin - releasing hormone release in response to low T3 levels; and changes in the central regulation of the thyroid axis, including decreased TSH pulsatility and changes in the peripheral components of the thyroid axis 17,38 .”
Ma, X., Wang, Y., Li, J., Lin, Z., Gong, P., Fei, J., Shu, M., Tao, Q., & Dai, P. (2026) · Research Square · doi:10.21203/rs.3.rs-8395613/v1
Li, L., Li, X., Liu, B., Yin, J., Yuan, M., & Yuan, M. (2026) · Risk Management and Healthcare Policy · doi:10.2147/rmhp.s575782
“4,5 9–11 However, the impact of AP on endocrine system remains inadequately characterized.”
Li, F., Zan, Y., Zhang, K., Liu, F., Si, B., Lin, L., Guo, J., Zhang, Q., Wang, D., & Xu, X. (2026) · Frontiers in Endocrinology · doi:10.3389/fendo.2026.1788453
Xue, B., Liu, Y., Wan, J., Tang, S., Shi, X., Cao, J., & Yuan, H. (2026) · Frontiers in Endocrinology · doi:10.3389/fendo.2026.1839913
“This process leads to direct oxidative damage and functional impairment of the deiodinase enzymes (32).”
Unilateral hilar sarcoidosis with anemia and low T3 syndrome: a case report
水跃翔, Wang, H., & Wang, S. (2026) · Frontiers in Medicine · doi:10.3389/fmed.2026.1892525
“It may also influence peripheral thyroid hormone metabolism and participate in low T3 syndrome during systemic illness (14, 15).”
Varmış, D. A., YÜKSEKKAYA, C., Binokay, H., Güneş, S., İNCE, N., Koçak, E., ANTEPÜZÜMÜ, E. G. Y., Sahin, K., & Tanrikulu, E. E. (2026) · Brain Sciences · doi:10.3390/brainsci16080776
Cho, S., Hwang, S. E., Yun, J. M., Kim, S. T., Kang, Y. H., Kim, H.-J., & Park, J. (2026) · Journal of Endocrinological Investigation · doi:10.1007/s40618-026-02965-6
“The disruption of the thyroid gland by oxidative stress and the hypothalamic-pituitary-thyroid axis through inflammatory markers, such as interleukin-6, has been reported to inhibit thyroxine activation [39].”
Pai, D., Sujir, S. N., Surkunda, S. T., Nisarg, S., & Kunju, S. A. (2026) · Research Square · doi:10.21203/rs.3.rs-10773566/v1
Cytokine and chemokine dysregulation by Endocrine Disrupting Chemicals (EDCs)
Franchi, E., Coperchini, F., Greco, A., Croce, L., Parisi, R., Denegri, M., & Rotondi, M. (2026) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2026.101530
Mudjanarko, S. W., Retnaningtyas, F. D., Oktavian, P., Thaha, M., Tjempakasari, A., & Kusumawindani, D. (2026) · Research Square · doi:10.21203/rs.3.rs-11029817/v1
Acute Endocrine Alterations After Traumatic Brain Injury and 6‐Month Functional Outcome
Xu, B., Guo, P., Pan, R., Wang, Z., Zhou, J., Zhang, P., Zhang, X., Zhang, Q., Ma, H., & Niu, Z. (2026) · Annals of Clinical and Translational Neurology · doi:10.21203/rs.3.rs-9597854/v1
Metadata
- Authors
- Wajner, S. M., Goemann, I. M., Bueno, A. L., Larsen, P. R., & Maia, A. L.
- Affiliations
- Universidade Federal do Rio Grande do Sul (BR)
- Brigham and Women's Hospital (US)
- Corresponding author
- Maia, Ana Luiza
- Venue
- Journal of Clinical Investigation
- Published
- 2011-05-02
- Volume
- 121
- Issue
- 5
- Pages
- 1834-1845
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC3083773
- OpenAlex
- W2114397821
- Cited by
- 168
- References
- 74
- Citations by year
- 2026: 14 · 2025: 11 · 2024: 13 · 2023: 13 · 2022: 13 · 2021: 10 · 2020: 11 · 2019: 6 · 2018: 15 · 2017: 13 · 2016: 18 · 2015: 9 · 2014: 6 · 2013: 6 · 2012: 8
- FWCI
- 5.77
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Dartmouth College
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
- Conselho Nacional de Desenvolvimento Científico e Tecnológico
- Fundação de Amparo à Pesquisa do Estado do Rio Grande do Sul
- Universidade Federal do Rio Grande do Sul
- Fundação Instituto de Pesquisas Econômicas
- National Institutes of Health
- Fogarty International Center (R03TW007559, TW007559)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK36256, R01DK036256)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Keywords
- low T3 syndrome, interleukin-6, thyroid hormone metabolism, deiodinases, type I deiodinase, type 2 deiodinase, type III deiodinase, triiodothyronine, thyroxine, oxidative stress, glutathione, N-acetylcysteine, cytokines, thyroid hormone inactivation
- MeSH terms
- Acetylcysteine, Cell Line, Dithiothreitol, Glutathione, Humans, RNA, Messenger, Thyroid Diseases, Thyroid Hormones, Thyroxine, Interleukin-6, Cytokines, Reactive Oxygen Species, Oxidative Stress, Cell Line, Tumor
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
