The impact of diabetes mellitus on tendon pathology: a review DOI Creative Commons
Jian Xu, Jinbo Wang,

Yuncong Ji

et al.

Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 15

Published: Nov. 5, 2024

Diabetes is one of the most common metabolic diseases worldwide, leading to complications, mortality, and significant healthcare expenditures, which impose a substantial social financial burden globally. A diabetic environment can induce changes, negatively affecting tendon homeostasis, alterations in biomechanical properties histopathology. Numerous studies have investigated mechanisms through diabetes exerts pathological effects on tendons, including increased free radical production, oxidative stress, inflammatory responses, deposition advanced glycation end products (AGEs), microvascular changes. These changes damages structure, biomechanics, repair processes. The proliferation stem cells decreases, apoptosis increases, abnormal differentiation, along with expression myofibroblasts, ultimately lead insufficient repair, fibrosis, remodeling. Although researches unveiling tendinopathy, fibrosis or contracture, injury healing are growing, systematic understanding still lacking. Therefore, this review summarizes current research status provides comprehensive overview, offering theoretical guidance for future in-depth exploration impact tendons development treatments diabetes-related diseases.

Language: Английский

Lipoic acid-plumbagin conjugate protects pancreatic beta cells against high glucose-induced toxicity DOI Creative Commons

Parveen Abdulhaniff,

Chitra Loganathan, Penislusshiyan Sakayanathan

et al.

Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)

Published: April 1, 2025

Pancreatic β cells that produce insulin play a significant role in maintaining glucose homeostasis. However, high (HG) causes oxidative stress, which leads to pancreatic cell dysfunction. The synthesis of lipoic acid (LA) and plumbagin (PLU) conjugate (LA-PLU) was done characterized using (1H) NMR, (13C) LC–ESI–MS/MS, UV–visible spectroscopy techniques. ADME analysis confirmed the drug-like properties LA-PLU. present study revealed protective effect LA-PLU against HG (25 mM)-induced stress on cells. Cell viability performed RIN-5F found exhibits non-toxic up 91.23 ± 2.61% at 12.5 µM concentration. At µM, protected 73.45 3.72% under conditions. showed HG-induced DNA damage, followed by preserving mitochondrial membrane potential decreasing reactive oxygen species formation. Further, an anti-apoptotic increasing Bcl-2 (B lymphoma-2) level apoptotic proteins [Bcl-2 associated x (Bax), cleaved caspase-3). Hence, overall concludes could act as potent antioxidant protects conditions, resulting maintenance

Language: Английский

Citations

0
Advances in cytokine-based herbal medicine against premature ovarian insufficiency: A review DOI
Siyu Yuan,

Zhu Shixiao,

Sun Congying

et al.

Journal of Ethnopharmacology, Journal Year: 2024, Volume and Issue: 333, P. 118477 - 118477

Published: June 21, 2024

Language: Английский

Citations

2
Osthole mitigates the myofibroblast properties in oral submucous fibrosis by suppressing the TGF-β/smad2 signaling pathway and NCK-AS1 expression DOI Creative Commons

Po-Yu Yang,

Pei‐Ling Hsieh,

Jung‐Chun Yeh

et al.

Journal of Dental Sciences, Journal Year: 2024, Volume and Issue: 20(2), P. 911 - 918

Published: Sept. 8, 2024

Natural products are gaining increasing recognition as an alternative source for alleviating fibrosis they can regulate various mediators or pathways against by targeting non-coding RNAs. In the current study, we aimed to investigate therapeutic effects of osthole in oral submucous (OSF), a precancerous condition cavity. The cytotoxicity normal and fibrotic buccal mucosal fibroblasts (fBMFs) derived from OSF tissues was assessed using MTT assay. Collagen gel contraction transwell migration assays were conducted examine myofibroblast activities. Besides, expression TGF-β/Smad2 signaling well α-SMA type I collagen measured. Additionally, RNA sequencing used identify potential target involved anti-fibrotic effect osthole. Osthole exhibited higher cytotoxic on fBMFs compared BMFs dose-dependently reduced several activities, including contractility ability. addition, pathway inhibited along with lower osthole-receiving cells. Moreover, administration downregulated NCK1-AS1 fBMFs, which proven mediate anti-fibrosis property Our results indicate that may be promising compound inhibit progression OSF.

Language: Английский

Citations

1
Targeting programmed cell death in diabetic kidney disease: from molecular mechanisms to pharmacotherapy DOI Creative Commons

Fengzhao Liu,

Zhenyu Yang, Jixin Li

et al.

Molecular Medicine, Journal Year: 2024, Volume and Issue: 30(1)

Published: Dec. 20, 2024

Abstract Diabetic kidney disease (DKD), one of the most prevalent microvascular complications diabetes, arises from dysregulated glucose and lipid metabolism induced by hyperglycemia, resulting in deterioration renal cells such as podocytes tubular epithelial cells. Programmed cell death (PCD), comprising apoptosis, autophagy, ferroptosis, pyroptosis, necroptosis, represents a spectrum demise processes intricately governed genetic mechanisms vivo. Under physiological conditions, PCD facilitates turnover cellular populations serves protective mechanism to eliminate impaired or cells, thereby preserving tissue homeostasis amidst hyperglycemic stress. However, existing research predominantly elucidates individual modes death, neglecting intricate interplay mutual modulation observed among various forms PCD. In this comprehensive review, we delineate diverse regulatory governing elucidate crosstalk dynamics distinct pathways. Furthermore, review recent advancements understanding pathogenesis explore their implications DKD. Additionally, potential natural products derived primarily botanical sources therapeutic agents, highlighting multifaceted effects on modulating crosstalk, proposing novel strategies for DKD treatment.

Language: Английский

Citations

1
The impact of diabetes mellitus on tendon pathology: a review DOI Creative Commons
Jian Xu, Jinbo Wang,

Yuncong Ji

et al.

Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 15

Published: Nov. 5, 2024

Diabetes is one of the most common metabolic diseases worldwide, leading to complications, mortality, and significant healthcare expenditures, which impose a substantial social financial burden globally. A diabetic environment can induce changes, negatively affecting tendon homeostasis, alterations in biomechanical properties histopathology. Numerous studies have investigated mechanisms through diabetes exerts pathological effects on tendons, including increased free radical production, oxidative stress, inflammatory responses, deposition advanced glycation end products (AGEs), microvascular changes. These changes damages structure, biomechanics, repair processes. The proliferation stem cells decreases, apoptosis increases, abnormal differentiation, along with expression myofibroblasts, ultimately lead insufficient repair, fibrosis, remodeling. Although researches unveiling tendinopathy, fibrosis or contracture, injury healing are growing, systematic understanding still lacking. Therefore, this review summarizes current research status provides comprehensive overview, offering theoretical guidance for future in-depth exploration impact tendons development treatments diabetes-related diseases.

Language: Английский

Citations

0