Role of Transforming Growth Factor-β in Skeletal Muscle Fibrosis: A Review

Ismaeel, Ahmed; Kim, Jeong‐Su; Kirk, Jeffrey S.; Smith, Robert S.; Bohannon, W. Todd; Koutakis, Panagiotis

doi:10.3390/ijms20102446

Cited by 101 publications

(105 citation statements)

References 87 publications

(134 reference statements)

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“…At the end of exposure, mRNA expression of TGF-β in renal tissues of the PM 2.5 group was increased. TGF-β plays an important role in participating in post-injury repair of tissues by promoting the deposition of extracellular matrix components such as collagen (Ismaeel et al, 2019). But prolonged, uncontrolled TGF-β activation can lead to an overdose of extracellular matrix, leading to tissue brosis (Rauchman and Griggs, 2019).…”

Section: Discussionmentioning

confidence: 99%

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Huang

Zhou

Liu

et al. 2020

Preprint

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Abstract Background: Exposure to airborne fine particulate matter (PM2.5) has been declared to be harmful to human kidney. However, whether activation of the autophagic pathway plays key roles in the nephrotoxicity caused by PM2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of kidney damage after PM2.5 exposure in vivo and in vitro.Results: In the present study, statistically significant alterations in water intake, urine flow rate and mean blood pressure were observed between the concentrated PM2.5 (PM2.5) group and the filtered air (FA) group. Exposed animals showed severe edema of renal tubular epithelial cells, capillary congestion, reduction of the glomerular urinary space and early pro-fibrotic state. Moreover, significant increases in the levels of early kidney damage markers were observed in the exposed rats and these animals exhibited more apoptosis rate in kidney cells. In addition, PM2.5 exposure activated the autophagic pathway, as evidenced by LC3-I to LC3-II conversion, activation of P62 and beclin-1. All of these effects are in concurrence with the presence of more autophagosomes both in vivo and in vitro after PM2.5 exposure. Conclusions: Taken together, our findings indicated that PM2.5-induced renal function impairment via the activation of the autophagic pathway in renal tubular epithelial cells.

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Section: Discussionmentioning

confidence: 99%

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Huang

Zhou

Liu

et al. 2020

Preprint

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show abstract

“…Myostatin is intrinsically linked to TGF-β [ 72 ]. TGF-β/myostatin activation has been widely studied in DMD [ 71 , 72 , 73 , 74 , 75 , 76 ]. GCs bind to SMAD and Daxx, and can interfere with satellite cell differentiation, which is detrimental to DMD patients.…”

Section: Activation Of the Cellular Pathways In Skeletal Muscle Cementioning

confidence: 99%

Anti-Inflammatory and General Glucocorticoid Physiology in Skeletal Muscles Affected by Duchenne Muscular Dystrophy: Exploration of Steroid-Sparing Agents

Herbelet

Rodenbach

Paepe

et al. 2020

IJMS

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In Duchenne muscular dystrophy (DMD), the activation of proinflammatory and metabolic cellular pathways in skeletal muscle cells is an inherent characteristic. Synthetic glucocorticoid intake counteracts the majority of these mechanisms. However, glucocorticoids induce burdensome secondary effects, including hypertension, arrhythmias, hyperglycemia, osteoporosis, weight gain, growth delay, skin thinning, cushingoid appearance, and tissue-specific glucocorticoid resistance. Hence, lowering the glucocorticoid dosage could be beneficial for DMD patients. A more profound insight into the major cellular pathways that are stabilized after synthetic glucocorticoid administration in DMD is needed when searching for the molecules able to achieve similar pathway stabilization. This review provides a concise overview of the major anti-inflammatory pathways, as well as the metabolic effects of glucocorticoids in the skeletal muscle affected in DMD. The known drugs able to stabilize these pathways, and which could potentially be combined with glucocorticoid therapy as steroid-sparing agents, are described. This could create new opportunities for testing in DMD animal models and/or clinical trials, possibly leading to smaller glucocorticoids dosage regimens for DMD patients.

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“…After the end of exposure, mRNA expression of TGF-β in renal tissues of the PM 2.5 group was increased. TGF-β plays an important role in participating in post-injury repair of tissues by promoting the deposition of extracellular matrix components such as collagen (Ismaeel et al, 2019). But prolonged, uncontrolled TGF-β activation can lead to an overdose of extracellular matrix, leading to tissue fibrosis (Rauchman and Griggs, 2019).…”

Section: Discussionmentioning

confidence: 99%

PM2.5 exposure induces renal injury via the activation of the autophagic pathway in rat and HK-2 cell

Huang

2020

Preprint

View full text Add to dashboard Cite

Background Exposure to airborne fine particulate matter (PM2.5) has been declared to be harmful to the human kidney. However, whether activation of the autophagic pathway plays key roles in the nephrotoxicity caused by PM2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of kidney damage after PM2.5 exposure in vivo and in vitro. Results In the present study, statistically significant alterations in water intake, urine flow rate and mean blood pressure were observed between the PM2.5 group and FA group during the period of PM2.5 exposure. Exposed animals showed severe edema of renal tubular epithelial cells, capillary congestion, reduction of the glomerular urinary space and early pro-fibrotic state. Moreover, significant increases in the levels of early kidney damage markers were observed in the exposed rats and these animals exhibited more apoptosis rate in kidney cells. In addition, PM2.5 exposure resulted in the activation of the autophagic pathway, as evidenced by LC3-I to LC3-II conversion, P62 and beclin-1 activated. All of these effects are in concurrence with the presence of more autophagosomes both in vivo and in vitro after PM2.5 exposure. Conclusions Taken together, our findings indicated that PM2.5-induced renal injury via the activation of the autophagic pathway in renal tubular epithelial cells.

show abstract

Role of Transforming Growth Factor-β in Skeletal Muscle Fibrosis: A Review

Cited by 101 publications

References 87 publications

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Anti-Inflammatory and General Glucocorticoid Physiology in Skeletal Muscles Affected by Duchenne Muscular Dystrophy: Exploration of Steroid-Sparing Agents

PM2.5 exposure induces renal injury via the activation of the autophagic pathway in rat and HK-2 cell

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