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Medicinal Potential of Fenugreek in Neuropathy and Neuroinflammation Associated Disorders
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Aman Upaganlawar, Chandrashekhar Upasani, Mayur B. Kale
Several studies confirm that fenugreek’s protective effects against DN’s development and progression are mediated by alleviating renal oxidative stress and suppressing the TGF-??1/CTGF signaling pathway and many other mechanisms (Jin et al. 2014; Sayed, Khalifa, and Abd El-Latif 2012) (Figure 14.1).
Pathogenesis
Published in Aparna Palit, Arun C. Inamadar, Systemic Sclerosis, 2019
CTGF demonstrates functions similar to TGF-β. Increased expression of CTGF in lesioned tissues of patients with SSc is mediated by TGF-β, hypoxia and ET-1. A variation in the promoter region of CTGF gene, which predisposes an individual to develop SSc, has been demonstrated.3 TGF-β stimulates FBs, vascular smooth muscles, and endothelial cells to secrete CTGF. Through the autocrine loop stimulation, CTGF maintains a continuous and prolonged cycle of fibrosis by stimulating its own production.1 The expression of another important growth factor, PDGF, is involved in fibrosis and endothelial injury and has been known to increase in the lungs, skin, and bronchoalveolar lavage fluid of SSC patients. PDGF promotes endothelial proliferation, ECM production, and the release of profibrotic mediators like IL-6 and MCP-1. The autocrine PDGF/PDGFRα signaling loop in FBs is dependent on TGF-β and IL-1α.3
Inflammatory Responses Acquired Following Environmental Exposures Are Involved in Pathogenesis of Musculoskeletal Pain
Published in Kohlstadt Ingrid, Cintron Kenneth, Metabolic Therapies in Orthopedics, Second Edition, 2018
Ritchie C. Shoemaker, James C. Ryan
Smad3 has a greater role acting on epithelial cells and fibroblasts [78] but also activates other transcription factors [79], including connective tissue growth factor (CTGF). CTGF is a major factor implicated in formation of fibrous tissues. Inhibition of TGF beta-1 can be accomplished. Such an effort will help illnesses as diverse as interstitial lung disease to scleroderma; and from cirrhosis to burn healing.
Perspectives on the advances in the pharmacotherapeutic management of Duchenne muscular dystrophy
Published in Expert Opinion on Pharmacotherapy, 2022
Kelsie D. Kracht, Nicole L. Eichorn, Daniel J. Berlau
Pamrevlumab is a monoclonal antibody that inhibits connective tissue growth factor (CTGF) to reduce fibrosis. CTGF has many roles, but of note, it mediates tissue remodeling and fibrosis. Fibrosis is a concern in the heart and lungs in DMD patients because it contributes to cardiomyopathy and loss of pulmonary function as the disease progresses. Preliminary data from the phase 2 trial, where it is assessing change in percent predicted forced vital capacity (ppFVC), gave enough evidence of preserved limb strength and improved heart and lung function for the FDA to fast track the medication (ClinicalTrials.gov identifier: NCT02606136) [81]. Pamrevlumab is being evaluated in phase 3 trials LELANTOS with the primary outcome of change in score of PUL from baseline and LELANTOS-2, evaluating the change in NSAA (ClinicalTrials.gov identifiers NCT04371666, NCT04632940). Pamrevlumab is expected to be evaluated for FDA approval in the next few years.
Selenium, a dietary-antioxidant with cardioprotective effects, prevents the impairments in heart rate and systolic blood pressure in adolescent rats exposed to binge drinking treatment
Published in The American Journal of Drug and Alcohol Abuse, 2021
M Luisa Ojeda, Paula Sobrino, Rui Manuel Rua, María del Carmen Gallego-Lopez, Fátima Nogales, Olimpia Carreras
The intermittent BD pattern used in adolescent rats increased all of the vascular markers studied herein. VEGF is considered the most potent proangiogenic growth factor involved in vascular permeability, vascular dilation, endothelial proliferation and angiogenesis. Previous data established that acute ethanol exposure significantly increases serum VEGF values, but also perturbs endothelial VEGF signaling and action (50,51). The growth factor CTGF plays important roles in cell adhesion, migration, proliferation, and angiogenesis and is critically involved in fibrotic process. Also, different studies have related CTGF to VEGF production and angiogenesis (52). CTGF is upregulated by stimuli involved in cardiovascular damage, including OS (53). Since ethanol exposure increases OS, both proteins (CTGF and VEGF) increased in the present study and endothelial function is compromised. Se supplementation improves vascular function, lowering SBP values by decreasing both parameters to normal values, probably due to its antioxidant properties. The observation of beneficial actions of Se on vascular function are not new, since anti-atherosclerotic activity of Se has been described previously (21).
Evaluation of aromatase inhibitor on radiation induced pulmonary fibrosis via TGF- β/Smad 3 and TGF- β/PDGF pathways in rats
Published in Toxicology Mechanisms and Methods, 2021
Shereen M. Elkiki, Heba H. Mansour, Lobna M. Anis, Hanan M. Gabr, Mona M. Kamal
Also, in the present study irradiation induced significant decrease in CTGF while in animals exposed to radiation with concurrent treatment with anastrozole CTGF shows significant increase compared to the corresponding group. (CTGF) not only is an essential mediator for the fibrotic activity of TGF-β but also can act independently of TGF-β. It can modulate the formation of myofibroblasts by regulating the transdifferentiation of fibroblasts or epithelial cells or by enabling edema leading to the deposition of provisional matrix on which the epithelial cells undergo epithelial-to-mesenchymal transition (EMT). CTGF stimulates myofibroblasts to express chemokines and cytokines that recruit leukocytes and regulate their activity and to deposit and remodel the extracellular matrix (ECM), leading to changes in organ structure and function (Bickelhaupt et al. 2017). Excessive ECM deposition results in scarring and thickening of the affected tissue, and interferes with tissue and organ homeostasis (Kelly et al. 2017). Either overexpression or knockdown of CTGF have no significant effects on TGF-β-dependent Smad2/3 phosphorylation or Smad3 transcriptional activity (Quan et al. 2010). These data indicate that the ability of endogenous CTGF to regulate type I procollagen expression is not dependent on direct potentiation of Smad activation in human dermal fibroblasts. So, CTGF action is Smad independent (Shi-Wen et al. 2006).