Diabetic nephropathy (DN) has become the most common secondary kidney disease causing end-stage renal disease (ESRD). Nevertheless, the underlying mechanisms responsible for DN remain largely unknown. Regulated in development and DNA damage response 1 (REDD1) is a prooxidative molecule known to contribute to diabetes mellitus and its complications. However, it has not been previously examined whether and how REDD1 can further drive renal tubular epithelial cell (RTEC) apoptosis and epithelial-to-mesenchymal transition in DN. The expression of REDD1 was elevated in the kidneys of DN patients and diabetic mice in this study. By generating the DN model in REDD1 knockout mice, we demonstrated that REDD1 deficiency significantly improved apoptosis and EMT in diabetic mice. In vitro experiments showed that REDD1 generation was induced by high glucose (HG) in HK-2 cells. Similarly, the transfection of REDD1 siRNA plasmid also suppressed HG-induced apoptosis and EMT. Furthermore, we discovered that the inhibition of REDD1 suppressed the expression of Nox4-induced HG and reactive oxygen species (ROS) synthesis in HK-2 cells. In addition, HG could induce endogenous REDD1 and TXNIP to form a powerful complex. In summary, our findings demonstrate that blocking the REDD1/TXNIP complex can prevent HG-induced apoptosis and EMT by inhibiting ROS production, highlighting REDD1 as a valuable therapeutic priority site for DN.

The placenta plays a crucial role in maintaining pregnancy stability, regulating fetal growth, and facilitating maternal–fetal exchange. Its proper development relies on placental vasculogenesis and angiogenesis, along with adaptive remodeling of the maternal uterine vasculature. However, the mechanisms underlying placental development and the successful establishment of the maternal–fetal interface remain incompletely understood. As the third gaseous signaling molecule identified after nitric oxide (NO) and carbon monoxide (CO), hydrogen sulfide (H₂S) has been demonstrated to regulate vascular adaptation during pregnancy by promoting angiogenesis and neovascularization. Dysregulated H₂S biosynthesis has been implicated in pregnancy complications, including preeclampsia (PE), fetal growth restriction (FGR), and preterm birth (PTB), underscoring its potential as a therapeutic target. Recent studies have revealed that H₂S regulates placental function via multiple signaling pathways, including activating adenosine triphosphate (ATP)-sensitive K+ (KATP) channels, large-conductance calcium-activated potassium channels (BKCa channels), endothelial nitric oxide synthase (eNOS) signaling, and mitochondrial dynamics. Notably, H₂S-mediated persulfidation of mitochondrial Rho GTPase 2 (Miro2) has been shown to maintain trophoblast invasiveness and promote placental vascular homeostasis. Additionally, exogenous H₂S donors (e.g., GYY4137 and NaHS) have demonstrated therapeutic potential in experimental models, effectively reversing PE-like pathologies, improving placental perfusion, and restoring trophoblast function. Research further indicates that BKCa channels play a key role in H₂S-mediated vasodilation by modulating intracellular Ca²⁺ flux, which influences placental vascular tone and perfusion, reinforcing the importance of H₂S in maternal–fetal circulation regulation. This review provides a comprehensive summary of H₂S biosynthesis and metabolism and its regulatory role in early placental development. Notably, elevated estrogen levels during pregnancy have been identified as key regulators of H₂S production, and we discuss the molecular mechanisms by which estrogen modulates H₂S synthesis. Furthermore, we discuss the vascular-protective and anti-inflammatory properties of H₂S donors and dual-donor strategies. As research continues to reveal H₂S-mediated mechanisms in placental function and pregnancy disorders, optimizing the pharmacological application and clinical translation of H₂S donors and combination therapies will be a key research focus. Advancing H₂S metabolic regulation, signaling pathways, and targeted delivery systems may drive the development of novel diagnostic tools and therapeutic strategies for pregnancy complications.

Objective: Chlamydia psittaci (Cps) feeds on gram-negative aerobic cells. Respiratory inhalation of Cps or close contact with infected animals can cause psittacosis in humans. Given its challengeable early diagnosis and rapid progression, misdiagnosis or improper antibacterial drugs may lead to multi-organ dysfunction with a high mortality. Case report: A pregnant woman at 29+1 weeks of gestational age had a fever. CT images of the chest showed lamellar consolidations in the inferior lobe of the right lung, light inflammation in the middle lobe of the right lung. Negative results were obtained from multiple times of blood and sputum culture. Next generation sequencing (NGS) results identified that Cps caused severe pneumonia, which was alleviated by specific antibiotic treatment. Conclusion: Cps can cause severe pneumonia in the pregnant woman and be cured through precise antibiotic treatment. NGS is efficient in the rapid identification of pathogens and accurate diagnosis when bacteriological culture fails. Objective: Chlamydia psittaci (Cps) feeds on gram-negative aerobic cells. Respiratory inhalation of Cps or close contact with infected animals can cause psittacosis in humans. Given its challengeable early diagnosis and rapid progression, misdiagnosis or improper antibacterial drugs may lead to multi-organ dysfunction with a high mortality. Case report: A pregnant woman at 29+1 weeks of gestational age had a fever. CT images of the chest showed lamellar consolidations in the inferior lobe of the right lung, light inflammation in the middle lobe of the right lung. Negative results were obtained from multiple times of blood and sputum culture. Next generation sequencing (NGS) results identified that Cps caused severe pneumonia, which was alleviated by specific antibiotic treatment. Conclusion: Cps can cause severe pneumonia in the pregnant woman and be cured through precise antibiotic treatment. NGS is efficient in the rapid identification of pathogens and accurate diagnosis when bacteriological culture fails.

The placenta is a pregnancy-specific organ, functioning as the maternal-fetal interface and mediating essential processes including exchange, protection, and endocrine regulation. Placental abnormalities contribute to the pathophysiology, onset, progression, and prognosis of major perinatal disorders, making imaging modalities that enable their detection and monitoring crucial. Ultrasound (US) imaging is the principal modality for placental imaging, providing structural assessment with B-mode and blood flow evaluation with Doppler mode. Furthermore, advanced techniques such as 3D power Doppler, quantitative US, and shear-wave elastography expand the capabilities of placental US imaging. Photoacoustic (PA) imaging enables observation of the optical properties of endogenous chromophores (e.g., hemoglobin) with high spatial resolution and measures blood oxygenation, a key factor in placental dysfunction, offering substantial value for placental imaging. In this review, we cover US/PA imaging techniques for placental imaging, including preclinical and clinical studies. In addition, by considering current limitations and potential solutions, we suggest future trajectories for the advancement of US/PA imaging in this field.