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Thyroid Hormone Therapy for Organ Repair: Present State, Problems and Future Vision

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A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 15294

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Special Issue Editor

Dr. Iordanis Mourouzis

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Guest Editor

Diabetes Center, First Department of Propaedeutic Internal Medicine, Medical School, National and Kapodistrian University of Athens, Laiko General Hospital, 11527 Athens, Greece
Interests: pharmacology; cardiac remodeling; cardiac regeneration; heart failure; sepsis; hypertension; atherogenesis
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Special Issue Information

Dear Colleagues,

Thyroid hormone (TH) is a critical regulator of essential biological processes and organ maturation during perinatal development. Later, in adult life, the availability of TH is critical for repair and recovery after injury. In this regard, low triiodothyronine (T3) levels are an independent strong predictor of disease outcome. Stressful stimuli (hypoxia, hyperglycemia, trauma, etc.) have been shown to trigger changes in the tissue TH signaling axis in different adult mammalian organs. This response provokes an adaptive/maladaptive process characterized by the reactivation of fetal developmental programs, structural remodeling, and pathological growth. Furthermore, a growing body of experimental and clinical evidence suggests that TH treatment may improve organ structure and function in disease and critical states, such as myocardial infarction, heart failure, brain ischemic stroke, multiple sclerosis, skeletal muscle trauma, sepsis, ARDS, and transplantation. This Special Issue will publish 1) novel experimental and clinical findings on the role of TH signaling and TH therapy in organ repair and 2) state-of-the-art reviews summarizing UpToDate evidence about the effects of TH therapy in different diseases and critical states. This Special Issue should pave the way for the clinical application of TH and thyroid analogs as novel therapeutic agents for organ repair.

Prof. Dr. Iordanis Mourouzis
Guest Editor

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Keywords

Thyroid hormone
Repair
Heart
Brain
Skeletal muscle
Kidney
Lungs

Published Papers (4 papers)

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Research

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12 pages, 6658 KiB

Open AccessArticle

Changes in Thyroid Hormone Signaling Mediate Cardiac Dysfunction in the Tg197 Mouse Model of Arthritis: Potential Therapeutic Implications

by Lydia Ntari, Polyxeni Mantzouratou, Athanasia Katsaouni, Constantinos Pantos, George Kollias and Iordanis Mourouzis

J. Clin. Med. 2021, 10(23), 5512; https://doi.org/10.3390/jcm10235512 - 25 Nov 2021

Cited by 2 | Viewed by 1523

Abstract

Background Rheumatoid Arthritis (RA) patients show a higher risk of heart failure. The present study investigated possible causes of cardiac dysfunction related to thyroid hormone (TH) signaling in a RA mouse model. Methods A TNF-driven mouse model of RA[TghuTNF (Tg197)] was used. Cardiac function was evaluated by echocardiography. SERCA2a and phospholamban protein levels in left ventricle (LV) tissue, thyroid hormone levels in serum, TH receptors in LV and TH-related kinase signaling pathways were measured. T3 hormone was administered in female Tg197 mice. Results We show LV and atrial dilatation with systolic dysfunction in Tg197 animals, accompanied by downregulated SERCA2a. We suggest an interaction of pro-inflammatory and thyroid hormone signaling indicated by increased p38 MAPK and downregulation of TRβ1 receptor in Tg197 hearts. Interestingly, female Tg197 mice showed a worse cardiac phenotype related to reduced T3 levels and Akt activation. T3 supplementation increased Akt activation, restored SERCA2a expression and improved cardiac function in female Tg197 mice. Conclusions TNF overexpression of Tg197 mice results in cardiac dysfunction via p38 MAPK activation and downregulation of TRβ1. Gender-specific reduction in T3 levels could cause the worse cardiac phenotype observed in female mice, while T3 administration improves cardiac function and calcium handling via modified Akt activation. Full article

(This article belongs to the Special Issue Thyroid Hormone Therapy for Organ Repair: Present State, Problems and Future Vision)

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6 pages, 458 KiB

Open AccessArticle

Hypovitaminosis D and Low T3 Syndrome: A Link for Therapeutic Challenges in Patients with Acute Myocardial Infarction

by Alessandro Pingitore, Francesca Mastorci, Sergio Berti, Laura Sabatino, Cataldo Palmieri, Giorgio Iervasi and Cristina Vassalle

J. Clin. Med. 2021, 10(22), 5267; https://doi.org/10.3390/jcm10225267 - 12 Nov 2021

Cited by 8 | Viewed by 1802

Abstract

Background and Aims: Vitamin D counteracts the reduction in the peripheral conversion of tiroxine (T4) into triiodothyronine (T3), which is the mechanism of low T3 syndrome (LT3) in acute myocardial infarction (AMI). The aim of this study was to assess the relationship between LT3 and hypovitaminosis D in AMI patients. Methods and Results: One hundred and twenty-four AMI patients were enrolled. Blood samples were taken at admission, and at 3, 12, 24, 48, and 72 h after admission. LT3 was defined as a value of fT3 ≤ 2.2 pg/mL, occurring within 3 days of hospital admission. Levels were defined as follows: sufficiency as a value of ±30 ng/mL, vitamin D insufficiency as 25-hydroxyvitamin D (25(OH)D) between 21 and 29 ng/mL, deficiency in 25(OH)D as below 20 ng/mL, and severe deficiency as values under 10 ng/mL. The percentage of subjects with severe 25(OH)D deficiency was significantly higher in the LT3 group (33% vs. 13%, p < 0.01). When LT3S was evaluated as a dependent variable, severe 25(OH)D deficiency (OR 2.6: 95%CI 1–6.7, p < 0.05) remained as an independent determinant after logistic multivariate adjustment together with age (>69 yrs, 50th percentile; OR 3.4, 95% CI 1.3–8.3, p < 0.01), but not female gender (OR 1.7, 95% CI 0.7–4.2, p = ns). Conclusions: This pilot study shows a relationship between hypovitaminosis D and LT3 in AMI patients. This association opens potential therapeutic challenges concerning the restoration of euthyroidism through vitamin D administration, together with the normalization of hypovitaminosis. Full article

(This article belongs to the Special Issue Thyroid Hormone Therapy for Organ Repair: Present State, Problems and Future Vision)

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Review

Jump to: Research

9 pages, 908 KiB

Open AccessReview

Thyroid Hormone Signalling in Human Evolution and Disease: A Novel Hypothesis

by Polyxeni Mantzouratou, Angelo Michele Lavecchia and Christodoulos Xinaris

J. Clin. Med. 2022, 11(1), 43; https://doi.org/10.3390/jcm11010043 - 23 Dec 2021

Cited by 6 | Viewed by 5761

Abstract

Thyroid hormone (TH) signalling is a universally conserved pathway with pleiotropic actions that is able to control the development, metabolism, and homeostasis of organisms. Using evidence from paleoecology/palaeoanthropology and data from the physiology of modern humans, we try to assess the natural history of TH signalling and its role in human evolution. Our net thesis is that TH signalling has likely played a critical role in human evolution by facilitating the adaptive responses of early hominids to unprecedently challenging and continuously changing environments. These ancient roles have been conserved in modern humans, in whom TH signalling still responds to and regulates adaptations to present-day environmental and pathophysiological stresses, thus making it a promising therapeutic target. Full article

(This article belongs to the Special Issue Thyroid Hormone Therapy for Organ Repair: Present State, Problems and Future Vision)

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18 pages, 596 KiB

Open AccessReview

Effects of Thyroid Hormone on Tissue Hypoxia: Relevance to Sepsis Therapy

by Athanasios I. Lourbopoulos, Iordanis S. Mourouzis, Athanasios G. Trikas, Ioulia K. Tseti and Constantinos I. Pantos

J. Clin. Med. 2021, 10(24), 5855; https://doi.org/10.3390/jcm10245855 - 14 Dec 2021

Cited by 12 | Viewed by 5602

Abstract

Tissue hypoxia occurs in various conditions such as myocardial or brain ischemia and infarction, sepsis, and trauma, and induces cellular damage and tissue remodeling with recapitulation of fetal-like reprogramming, which eventually results in organ failure. Analogies seem to exist between the damaged hypoxic and developing organs, indicating that a regulatory network which drives embryonic organ development may control aspects of heart (or tissue) repair. In this context, thyroid hormone (TH), which is a critical regulator of organ maturation, physiologic angiogenesis, and mitochondrial biogenesis during fetal development, may be of important physiological relevance upon stress (hypoxia)-induced fetal reprogramming. TH signaling has been implicated in hypoxic tissue remodeling after myocardial infarction and T3 prevents remodeling of the postinfarcted heart. Similarly, preliminary experimental evidence suggests that T3 can prevent early tissue hypoxia during sepsis with important physiological consequences. Thus, based on common pathways between different paradigms, we propose a possible role of TH in tissue hypoxia after sepsis with the potential to reduce secondary organ failure. Full article

(This article belongs to the Special Issue Thyroid Hormone Therapy for Organ Repair: Present State, Problems and Future Vision)

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