The authors analyzed ultrastructural changes in hepatocytes of weanling rats, induced by allyl alcohol (0.03 ml/kg). The most severe lesions developed in mitochondria of the periportal field of liver lobules during the first 24 hours following alcohol administration. Early signs of the regeneration were also seen in the periportal field 24 hours after exposure. Three types of dark hepatocytes were distinguished: (1) polygonal cells with the dilated endoplasmic reticulum, increased size and number of mitochodria; (2) stellate cells with the remarkably increased rough endoplasmic reticulum showing free ribosomes and a lot of large mitochondria; (3) cells consisting of irregularly arranged rough endoplasmic reticulum and a great number of small mitochondria. Large hepatocytes containing an insignificant number of organellas were seen in the later stages of the regeneration. The data obtained warranted a suggestion that the cells described represent different phases of hepatocytic regeneration.
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J Nephrol
January 2025
Department of Nephrology and Transplantation, Beaumont Hospital, Dublin, Ireland.
Background: Autosomal Dominant Polycystic Kidney Disease (ADPKD) represents the most common monogenic cause of kidney failure. While identifying genetic variants predicts disease progression, characterization of recently described ADPKD-like variants is limited. We explored disease progression and genetic spectrum of genetically-confirmed ADPKD families with PKD1 and non-PKD1 variants.
View Article and Find Full Text PDFNon-alcoholic fatty liver disease (NAFLD) is a prevalent metabolic liver disorder worldwide, and effective therapeutic strategies for its treatment remains limited. In this article, we introduced Glipo-siRubi, a hepatocytes-targeting RNA interference (RNAi) nanoliposome for suppression of Rubicon expression, aiming to achieve precise regulation of autophagy in NAFLD. Autophagy activation induced by Rubicon suppression resulted in reduced endoplasmic reticulum stress and intracellular lipid accumulation in vitro.
View Article and Find Full Text PDFJ Orthop Surg Res
January 2025
Linyi People's Hospital postgraduate training base of Guangzhou University of Traditional Chinese Medicine, Linyi, Shandong, 276000, China.
Background: The endoplasmic reticulum stress (ER stress) has been involved in various musculoskeletal disorders including non-traumatic osteonecrosis of femoral head (NT-ONFH).
Objective: The current study aimed to investigate the association of glucose-regulated protein 78 (GRP78) as well as CCAAT/enhancer-binding protein homologous protein (CHOP) expressions in serum and femoral head (FH) tissues with NT-ONFH's severity.
Methods: We enrolled NT-ONFH patients (n = 150) alongside healthy controls (HCs, n = 150).
Mol Med
January 2025
The First People's Hospital of Lin'an District, No. 360, Yikang Street, Jinnan Subdistrict, Lin'an District, Hangzhou, Zhejiang, 311300, China.
Background: Myocardial infarction (MI) remains a leading cause of mortality globally, often resulting in irreversible damage to cardiomyocytes. Ferroptosis, a recently identified form of regulated cell death driven by iron-dependent lipid peroxidation, has emerged as a significant contributor to post-MI cardiac injury. The endoplasmic reticulum (ER) stress response has been implicated in exacerbating ferroptosis.
View Article and Find Full Text PDFNat Chem Biol
January 2025
Zhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, China.
As an enzyme with a critical role in de novo purine synthesis, adenylosuccinate lyase (ADSL) expression is upregulated in various malignancies. However, whether ADSL possesses noncanonical functions that contribute to cancer progression remains poorly understood. Here, we demonstrate that protein kinase R-like endoplasmic reticulum kinase (PERK) activated by lipid deprivation or ER stress phosphorylates ADSL at S140, leading to an enhanced association between ADSL and Beclin1.
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