LOX-induced tubulointerstitial fibrosis via the TGF-β/LOX/Snail axis in diabetic mice DOI Creative Commons

Yicheng Lu,

Heyangzi Li,

Mohan Chen

и другие.

Journal of Translational Medicine, Год журнала: 2025, Номер 23(1)

Опубликована: Янв. 9, 2025

The partial epithelial-mesenchymal transition (EMT) is emerging as a significant mechanism in diabetic nephropathy (DN). LOX copper amine oxidase conventionally thought to act by crosslinking collagen. However, the role of EMT and fibrotic progression has not been investigated experimentally. bulk RNA sequencing single-nuclei (snRNA-seq) analysis were explored find nephropathy. We then possible signaling pathway LOX, both vivo vitro inhibition experiments mice HK-2 cells. Besides, we further assessed kidney fibrosis renal function. expression was elevated kidneys mice. Additionally, snRNA-seq results indicated that higher proximal tubular (PemtPT) epithelial Moreover, found increased prompted cells (RTECs) modulating transcription factor Snail vitro. Remarkably, effectively mitigated RTECs mice, thereby attenuating enhancing identified TGF-β an upstream regulator inhibiting partially reversed program induced pathway. Hyperglycemia induces via TGF-β/LOX/Snail axis, contributing fibrosis. Inhibiting can reverse RTECs, diminish fibrosis, improve

Язык: Английский

LOXL4, but not LOXL2, is the critical determinant of pathological collagen cross-linking and fibrosis in the lung DOI Creative Commons
Hsiao‐Yen Ma, Qingling Li, Weng Ruh Wong

и другие.

Science Advances, Год журнала: 2023, Номер 9(21)

Опубликована: Май 26, 2023

Idiopathic pulmonary fibrosis is a progressive fibrotic disease characterized by excessive deposition of (myo)fibroblast produced collagen fibrils in alveolar areas the lung. Lysyl oxidases (LOXs) have been proposed to be central enzymes that catalyze cross-linking fibers. Here, we report that, while its expression increased lungs, genetic ablation LOXL2 only leads modest reduction pathological but not On other hand, loss another LOX family member, LOXL4, markedly disrupts and Furthermore, knockout both Loxl2 Loxl4 does offer any additive antifibrotic effects when compared deletion only, as LOXL4 deficiency decreases members including Loxl2. basis these results, propose main activity underlying lung fibrosis.

Язык: Английский

Процитировано

28

Crosstalk between T lymphocyte and extracellular matrix in tumor microenvironment DOI Creative Commons

Die Lv,

Yujie Fei,

Hongli Chen

и другие.

Frontiers in Immunology, Год журнала: 2024, Номер 15

Опубликована: Апрель 16, 2024

The extracellular matrix (ECM) is a complex three-dimensional structure composed of proteins, glycans, and proteoglycans, constituting critical component the tumor microenvironment. Complex interactions among immune cells, matrix, cells promote development metastasis, consequently influencing therapeutic efficacy. Hence, elucidating these interaction mechanisms pivotal for precision cancer therapy. T lymphocytes are an important system, exerting direct anti-tumor effects by attacking or releasing lymphokines to enhance effects. ECM significantly influences function infiltration within microenvironment, thereby impacting behavior biological characteristics cells. involved in regulating synthesis, degradation, remodeling through secretion cytokines enzymes. As result, it affects proliferation invasive ability as well efficacy immunotherapy. This review discusses underlying lymphocyte-ECM microenvironment their potential application It provides novel insights innovative strategies drug.

Язык: Английский

Процитировано

15

Diverse interactions between AIEgens and biomolecules/organisms: Advancing from strategic design to precision theranostics DOI
Qihang Ding, Xiaoyu Xu, Yang Li

и другие.

Chem, Год журнала: 2024, Номер 10(7), С. 2031 - 2073

Опубликована: Июль 1, 2024

Язык: Английский

Процитировано

15

Delivery Strategy to Enhance the Therapeutic Efficacy of Liver Fibrosis via Nanoparticle Drug Delivery Systems DOI
Jie Liu,

Jinhu Liu,

Weiwei Mu

и другие.

ACS Nano, Год журнала: 2024, Номер 18(32), С. 20861 - 20885

Опубликована: Июль 31, 2024

Liver fibrosis (LF) is a pathological repair reaction caused by chronic liver injury that affects the health of millions people worldwide, progressing to life-threatening cirrhosis and cancer without timely intervention. Due complexity LF pathology, multiple etiological characteristics, deposited extracellular matrix, traditional drugs cannot reach appropriate targets in time-space matching way, thus decreasing therapeutic effect. Nanoparticle drug delivery systems (NDDS) enable multidrug co-therapy develop multifactor strategies targeting processes, showing great potential therapy. Based on pathogenesis current clinical treatment status LF, we systematically elucidate mechanism NDDS used LF. Subsequently, focus progress applications for including combined fibrotic environment, overcoming biological barriers, precise intracellular regulation, intelligent responsive microenvironment. We hope this review will inspire rational design future order provide ideas methods promoting regression cure.

Язык: Английский

Процитировано

14

LOX-induced tubulointerstitial fibrosis via the TGF-β/LOX/Snail axis in diabetic mice DOI Creative Commons

Yicheng Lu,

Heyangzi Li,

Mohan Chen

и другие.

Journal of Translational Medicine, Год журнала: 2025, Номер 23(1)

Опубликована: Янв. 9, 2025

The partial epithelial-mesenchymal transition (EMT) is emerging as a significant mechanism in diabetic nephropathy (DN). LOX copper amine oxidase conventionally thought to act by crosslinking collagen. However, the role of EMT and fibrotic progression has not been investigated experimentally. bulk RNA sequencing single-nuclei (snRNA-seq) analysis were explored find nephropathy. We then possible signaling pathway LOX, both vivo vitro inhibition experiments mice HK-2 cells. Besides, we further assessed kidney fibrosis renal function. expression was elevated kidneys mice. Additionally, snRNA-seq results indicated that higher proximal tubular (PemtPT) epithelial Moreover, found increased prompted cells (RTECs) modulating transcription factor Snail vitro. Remarkably, effectively mitigated RTECs mice, thereby attenuating enhancing identified TGF-β an upstream regulator inhibiting partially reversed program induced pathway. Hyperglycemia induces via TGF-β/LOX/Snail axis, contributing fibrosis. Inhibiting can reverse RTECs, diminish fibrosis, improve

Язык: Английский

Процитировано

2