Results 121 to 130 of about 94,921 (285)
The loss of Ubiquitin Specific Peptidase 26 (USP26) in osteoblasts results in decreased bone formation, as well as multi‐organ fibrosis associated with insulin resistance (IR). Mechanistically, the absence of USP26 reduces glycolysis and lactate accumulation, leading to decreased histone H3 lysine 18 lactylation (H3K18LA) in the promoter region of KH ...
Jiyuan Tang +9 more
wiley +1 more source
The NADPH oxidase NOX4 regulates redox and metabolic homeostasis preventing HCC progression
Loss of NOX4 in HCC tumor cells induces metabolic reprogramming in a Nrf2/MYC‐dependent manner to promote HCC progression. Abstract Background and Aims The NADPH oxidase NOX4 plays a tumor‐suppressor function in HCC. Silencing NOX4 confers higher proliferative and migratory capacity to HCC cells and increases their in vivo tumorigenic potential in ...
Irene Peñuelas‐Haro +14 more
wiley +1 more source
Schematic illustration demonstrating that hepatic Mettl3 depletion significantly elevates the secretion of Mif and Csf1. This elevation facilitates Trem2+ macrophage infiltration and triggers cholangiocyte remodeling through the Spp1‐Cd44 interaction, resulting in spontaneous PSC development in vivo.
Wenting Pan +19 more
wiley +1 more source
Adaptive mitochondrial mechanisms allow mitochondrial resilience and prevent the worsening of fibrosis, while deregulation of these mechanisms promotes the progression from no/minimal‐mild (F0‐F2) fibrosis to advanced fibrosis and cirrhosis (F3‐F4). Abstract Background and Aims Hepatitis B virus (HBV) infection causes oxidative stress (OS) and alters ...
Dimitri Loureiro +17 more
wiley +1 more source
Gli1+ adventitial stem cells (ASCs) have been thought to generate smooth muscle cells (SMCs) in atherosclerosis. Using a dual‐recombinase lineage tracing to exclude ectopic labeling, Wang et al. found that Gli1+ ASCs do not contribute to SMCs in atherosclerotic plaques.
Haixiao Wang +11 more
wiley +1 more source
Interleukin‐18 signaling promotes activation of hepatic stellate cells in mouse liver fibrosis
Interleukin‐18 signaling promotes activation of hepatic stellate cells in mouse liver fibrosis. Abstract Background and Aims Nucleotide‐binding oligomerization domain‐like receptor‐family pyrin domain‐containing 3 (NLRP3) inflammasome activation has been shown to result in liver fibrosis.
Jana Knorr +19 more
wiley +1 more source
Epigenetic silencing of SOCS3 expression contributes to fibrosis in Crohn’s disease [PDF]
Identified risk polymorphisms affecting the Jak-STAT3 pathway in patients with Crohn’s disease could affect TGF-β1 and collagen I expression and in the pathway’s negative regulator, SOCS3.
Kuemmerle, John F +2 more
core +1 more source
This study presents a 3D lymphoid tissue model engineered from adipose‐derived stem cells differentiated into fibroblastic reticular cell–like networks and co‐cultured with immune cells. The engineered system successfully generates antigen‐specific antibodies and cytokine responses, providing a platform for studying adaptive immunity, vaccine efficacy,
Mei ElGindi, Shaza Karaman, Jeremy Teo
wiley +1 more source
Lrat+ quiescent hepatic stellate cells (qHSC) give rise to Lrat+Fbln2+ activated HSC (aHSC) in alcohol‐associated hepatitis and this subpopulation is highly profibrotic, inflammatory, and immunoregulatory based on their single cell transcriptomic profile. Abstract Background and Aims Relative roles of HSCs and portal fibroblasts in alcoholic hepatitis (
Steven Balog +12 more
wiley +1 more source
Solid predominant lung adenocarcinoma exhibits an immune‐excluded, ferroptosis‐resistant niche enriched with IL4I1⁺ TAMs and TDO2⁺ myCAFs. Spatial and multi‐omics analyses reveal AhR‐driven crosstalk that promotes T cell exhaustion and therapy resistance. Blocking AhR with CH‐223191 restores ferroptosis sensitivity, and its combination with ferroptosis
Zhaoxuan Wang +16 more
wiley +1 more source

