Iodine is an essential micronutrient that is required for thyroid hormone (TH) synthesis. However, adequate maternal thyroid function is critical for fetal growth and neurodevelopment. Pregnancy increases iodine requirements due to enhanced renal clearance, higher maternal TH production, and transplacental transfer, making pregnant women especially vulnerable to iodine deficiency. In this review, we examine the molecular mechanisms of TH synthesis and regulation, placental transport and metabolism, and the physiological adaptations of thyroid function during gestation. We also analyze the clinical and public health consequences of iodine imbalances, ranging from deficiency to excess. Evidence indicates that mild iodine deficiency—which is common even in developed countries—can lead to maternal thyroid overstimulation, increased thyroglobulin levels, altered T3/T4 ratios, and enlarged thyroid volume, while severe deficiency results in maternal and fetal hypothyroidism with irreversible neurocognitive impairment in the offspring. Conversely, excessive iodine intake may impair fetal thyroid function through mechanisms such as the Wolff–Chaikoff effect. In conclusion, ensuring balanced iodine intake through iodized salt, supplementation, and routine thyroid monitoring during pregnancy is essential to protect maternal health and optimize early neurodevelopment.

Iodine is a crucial component of thyroid hormones (THs), specifically triiodothyronine (T3) and thyroxine (T4) and is vital for normal thyroid function. During pregnancy, a deficiency in iodine can result in inadequate production of THs, leading to hypothyroidism. This con-dition can negatively impact the intellectual development of the newborn. Numerous stud-ies have demonstrated that iodine deficiency during pregnancy correlates with lower IQ levels in children. This deficiency can hinder critical processes such as neurogenesis, neu-ronal migration, and myelination, all of which are essential for proper cognitive develop-ment. Research indicates that children born to iodine-deficient mothers are at a higher risk of having lower IQs compared to those whose mothers received iodine supplements during pregnancy. Therefore, ensuring sufficient iodine levels and optimal TH function during pregnancy is crucial for the cognitive development of children. This highlights the im-portance of nutrition and regular monitoring of thyroid health in pregnant women. This re-view focuses on the key mechanisms of thyroid hormone homeostasis and discusses the implications of iodine deficiency during pregnancy.

The origin of life possibly required processes in confined systems that facilitated simple chemical reactions and other more complex reactions impossible to achieve under the condition of infinite dilution. In this context, the self-assembly of micelles or vesicles derived from prebiotic amphiphilic molecules is a cornerstone in the chemical evolution pathway. A prime example of these building blocks is decanoic acid, a short-chain fatty acid capable of self-assembling under ambient conditions. This study explored a simplified system made of decanoic acids under temperatures ranging from 0 °C to 110 °C to replicate prebiotic conditions. The study revealed the first point of aggregation of decanoic acid into vesicles and examined the insertion of a prebiotic-like peptide in a primitive bilayer. The information gathered from this research provides critical insights into molecule interactions with primitive membranes, allowing us to understand the first nanometric compartments needed to trigger further reactions that were essential for the origin of life.

Thyroxine (T4) is a drug extensively utilized for the treatment of hypothyroidism. However, the oral absorption of T4 presents certain limitations. This research investigates the efficacy of CO₂ nanobubbles in water as a potential oral carrier for T4 administration to C57BL/6 hypothyroid mice. Following 18 h of fasting, the formulation was administered to the mice, demonstrating that the combination of CO₂ nanobubbles and T4 enhanced the drug’s absorption in blood serum by approximately 40%. To comprehend this observation at a molecular level, we explored the interaction mechanism through which T4 engages with the CO₂ nanobubbles, employing molecular simulations, semi-empirical quantum mechanics, and PMF calculations. Our simulations revealed a high affinity of T4 for the water–gas interface, driven by additive interactions between the hydrophobic region of T4 and the gas phase and electrostatic interactions of the polar groups of T4 with water at the water–gas interface. Concurrently, we observed that at the water–gas interface, the cluster of T4 formed in the water region disassembles, contributing to the drug’s bioavailability. Furthermore, we examined how the gas within the nanobubbles aids in facilitating the drug’s translocation through cell membranes. This research contributes to a deeper understanding of the role of CO₂ nanobubbles in drug absorption and subsequent release into the bloodstream. The findings suggest that utilizing CO₂ nanobubbles could enhance T4 bioavailability and cell permeability, leading to more efficient transport into cells. Additional research opens the possibility of employing lower concentrations of this class of drugs, thereby potentially reducing the associated side effects due to poor absorption.

Prevalence of autism spectrum disorder (ASD) has increased over the past three decades. In this regard, there is growing evidence suggesting that environmental factors during pregnancy may contribute as risk factors for ASD, potentially playing a role in this rising trend. Gestational hypothyroxinemia (HTX) is an asymptomatic and frequent thyroid condition characterized by low levels of thyroxine (T4) in blood, with normal range of T3 and TSH. When this condition occurs in early pregnancy it impairs fetal neurodevelopment and diminishes cognitive capacities in the offspring. Additionally, retrospective human studies have shown that gestational HTX is associated with autistic outcomes in the offspring, however, there is an absence of knowledge about the cellular and molecular autism-like traits in the offspring gestated under gestational HTX (HTX-offspring). In this work, autistic-like phenotypes were evaluated in HTX-offspring, using a mouse model of gestational HTX. Consistent with autism-like behaviors of mice models, HTX-offspring exhibited anxiety-related behavior and impaired social interaction skills. Similar to humans, these features were more pronounced in male HTXoffspring. At the molecular level, the expression of NLGN3 and HOMER1 was increased in the prefrontal cortex and hippocampus of male HTX-offspring, compared to the offspring gestated under euthyroidism. Moreover, HTX-offspring showed increased proinflammatory cytokines in serum and an increased ratio of Th17 lymphocytes relative to T regulatory lymphocytes (Th17/Treg), as well as high neuroinflammatory-like traits in the prefrontal cortex and hippocampus, which were also more pronounced in male HTX-offspring. Notably, by administering T4 to pregnant mice during the induction of HTX, the offspring was protected from developing the observed autism-like traits. These findings support that gestational HTX constitutes a significant risk factor for the development of autism-like phenotypes in the offspring and strongly emphasizes the importance of monitoring thyroid function in early pregnancy.

Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a premier model for precision medicine, having moved from genetic discovery to approved therapeutics within two decades. Yet despite the clinical success of monoclonal antibodies, small interfering RNA and the newly approved oral macrocyclic-peptide inhibitor class, targeting PCSK9 remains a demanding biophysical challenge. Clinical translation has concentrated almost entirely on the rigid, well-resolved subtilisin-like catalytic domain that interfaces with the low-density lipoprotein receptor (LDLR). By contrast, the C-terminal cysteine- and histidine-rich domain (CHRD), which governs allosteric regulation, protein trafficking and post-translational modification, is highly disordered and largely elusive in experimental structures, leaving a critical regulatory network therapeutically unexploited. This review examines how advanced computational biology is bridging that structural gap, organizing the computational landscape of PCSK9 around the biophysical mechanisms of gain- and loss-of-function variants. We detail how explicit-solvent molecular dynamics, free-energy calculations and cryptic-pocket detection expose the functional plasticity and allosteric networks that static crystallography cannot capture, and we evaluate the convergence of these physics-based approaches with artificial intelligence, including deep-learning structure prediction and generative design of de novo nanobody and peptide binders. Therapeutic development and the structural literature currently point in diverging directions: drug discovery remains focused on the crowded LDLR-binding interface, whereas computational methods are beginning to identify candidate sites beyond it. We argue that the next advance in PCSK9 therapeutics will come from integrating generative artificial intelligence with rigorous enhanced sampling in a unified pipeline, deliberately shifting focus toward the disordered regulatory domains that have evaded classical screening.