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The most common hereditary disorder in adults, α1-antitrypsin deficiency (AATD), is characterized by reduced plasma levels or the abnormal functioning of α1-antitrypsin (AAT), a major human blood serine protease inhibitor, which is encoded by the SERine Protein INhibitor-A1 () gene and produced in the liver. Recently, it has been hypothesized that the geographic differences in COVID-19 infection and fatality rates may be partially explained by ethnic differences in allele frequencies. In our review, we examined epidemiological data on the correlation between the distribution of AATD, SARS-CoV-2 infection, and COVID-19 mortality rates. Moreover, we described shared pathogenetic pathways that may provide a theoretical basis for our epidemiological findings. We also considered the potential use of AAT augmentation therapy in patients with COVID-19.
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http://dx.doi.org/10.3390/jcm10194493 | DOI Listing |
Clin Oral Investig
September 2025
Department of Stomatology, Shengli Oilfield Central Hospital, No. 31, Jinan Road, Dongying, 257034, China.
Objective: Progesterone (PG) and its target, progesterone receptor (PGR), are important regulators in inflammatory diseases. This study aimed to investigate the specific role of PG in periodontitis and to elucidate the underlying mechanisms involving PGR.
Methods: Women with periodontitis, including 250 with PG deficiency, 250 with PG supplementation, and 245 controls (normal PG) were enrolled.
Virchows Arch
September 2025
Department of Public Health, University Federico II of Naples, Naples, Italy.
The PTEN tumor suppressor regulates the PIK3CA/AKT1 pathway, and its inactivation significantly contributes to tumorigenesis and progression in hormone receptor-positive/HER2-negative (HR + /HER2 -) metastatic breast cancer (MBC). In ~ 5% of these patients, PTEN loss, primarily due to gene deletions, leads to aberrant PI3K signaling and enhanced oncogenic potential. Findings from the CAPItello-291 study further establish PTEN together with PIK3CA and AKT1 as a predictive biomarker for Capivasertib, a pan-AKT inhibitor, in these patients.
View Article and Find Full Text PDFCell Death Differ
September 2025
Graduate Institute of Physiology, College of Biomedical Sciences, National Defense Medical University, Taipei, Taiwan, Republic of China.
Peroxisome proliferator-activated receptor alpha (PPARα) is a crucial transcriptional factor that regulates fatty acid β-oxidation and ketogenesis in response to fasting. However, the mechanisms underlying PPARα function remain unclear. This study identified a novel PPARα-binding protein-RING finger protein 128 (RNF128)-that facilitates PPARα polyubiquitination, resulting in the degradation and suppression of PPARα function during fasting.
View Article and Find Full Text PDFNat Aging
September 2025
State Key Laboratory of Conservation and Utilization of Bio-resources in Yunnan and Center for Life Sciences, School of Life Sciences, Yunnan University, Kunming, China.
Membraneless organelles assembled by liquid-liquid phase separation interact with diverse membranous organelles to regulate distinct cellular processes. It remains unknown how membraneless organelles are engaged in mitochondrial homeostasis. Here we demonstrate that mitochondria-associated translation organelles (MATOs) mediate local synthesis of proteins required for structural and functional maintenance of mitochondria.
View Article and Find Full Text PDFCell Mol Immunol
September 2025
School of Chinese Medicine, the University of Hong Kong, Hong Kong SAR, China.
Type I interferon (IFN-I) is highly prevalent in autoimmune disorders and is intricately involved in disease pathogenesis, including Sjögren's disease (SjD), also known as Sjögren's syndrome. Although the T follicular helper (Tfh) cell response has been shown to drive SjD development in a mouse model of experimental Sjögren's syndrome (ESS), the connection between IFN-I and the Tfh cell response remains unclear. As the activation of stimulator of interferon genes (STING) induces IFN-I production, we first demonstrated that mice deficient in STING or IFN-I signaling presented diminished Tfh cells and were completely resistant to ESS development.
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