Chronic Alcohol Ingestion and Predisposition to Lung “Cirrhosis”

Roman, Jesse

doi:10.1111/acer.12335

Cited by 3 publications

(3 citation statements)

References 23 publications

(29 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A number of biochemical and mechanical factors have been implicated in promoting fibrotic diseases. Along these lines, an enhanced production of collagen I and/or III has been noted in EtOHinduced pathological conditions [Law and Carver, 2013;El Hajj et al, 2014;Roman, 2014]. In the present study, EtOH increased collagen type I A1 chain content in C2C12 myocytes.…”

Section: Discussionsupporting

confidence: 77%

Adamts1 Mediates Ethanol‐Induced Alterations in Collagen and Elastin via a FoxO1‐Sestrin3‐AMPK Signaling Cascade in Myocytes

Hong-Brown

Brown

Navaratnarajah

et al. 2014

J of Cellular Biochemistry

View full text Add to dashboard Cite

A variety of stressors including alcohol (EtOH) are known to induce collagen production and fibrotic diseases. Matrix metalloproteinases (MMP) play an important role in regulating fibrosis, but little is known regarding the relationship between EtOH and MMPs. In addition, the signaling cascades involved in this process have not been elucidated. We have identified the MMP Adamts1 as a target of EtOH regulation. To characterize the function of Adamts1, we examined EtOH-induced alterations in collagen I and elastin protein levels in C2C12 myocytes. Incubation of myocytes with 100 mM EtOH decreased elastin and increased collagen content, respectively, and these changes were associated with increased O-GLcNAc modification of Adamts1. Conversely, silencing of Adamts1 by siRNA blocked the adverse effects of EtOH on collagen and elastin levels. Similar results were obtained after treatment with a pharmacological inhibitor of MMP. Changes in collagen were due, at least in part, to a decreased interaction of Adamts1 with its endogenous inhibitor TIMP3. The AMPK inhibitor compound C blocked the EtOH-induced stimulation of collagen and O-GLcNAc Adamts1 protein. Changes in AMPK appear linked to FoxO1, since inhibition of FoxO1 blocked the effects of EtOH on AMPK phosphorylation and O-GLcNAc levels. These FoxO-dependent modifications were associated with an upregulation of the FoxO1 transcription target sestrin 3, as well as increased binding of sestrin 3 with AMPK. Collectively, these data indicate that EtOH regulates the collagen I and elastin content in an Adamts1-dependent manner in myocytes. Furthermore, Adamts1 appears to be controlled by the FoxO1-sestrin 3-AMPK signaling cascade.

show abstract

Section: Discussionsupporting

confidence: 77%

Adamts1 Mediates Ethanol‐Induced Alterations in Collagen and Elastin via a FoxO1‐Sestrin3‐AMPK Signaling Cascade in Myocytes

Hong-Brown

Brown

Navaratnarajah

et al. 2014

J of Cellular Biochemistry

View full text Add to dashboard Cite

show abstract

“…Chronic alcohol intake increased lung fibrosis in the bleomycin-model of lung injury, as this effect was related to increased production of transforming growth factor β (TGFβ) and expression of α-smooth muscle actin suggests that the lung is a target for alcohol, and that chronic alcohol intake may predispose the lung to disrepair after injury (38). The overexpression of pro-fibrotic growth factors and pro-inflammatory cytokines, and the generation of oxidant stress may lead to lung cellular dysfunction, aberrant tissue remodelling and loss of lung function (38).…”

Section: Impact On the Brainmentioning

confidence: 99%

Chronic Alcohol Use and Accompanying Noncommunicable Diseases

Ayenigbara

2020

Croat. nurs. j. (Online)

View full text Add to dashboard Cite

Introduction. Heavy and chronic alcohol use connotes frequent, continuous and persistent consumption of alcoholic drinks over an extended period of time. Importantly, heavy consumption of alcohol causes many health problems to the drinker and the society at large, as over 5.1% of the global burden of morbidity and injuries are attributable to alcohol usage alone. Aim. The purpose of this study is to identify some of the noncommunicable diseases that are associated with chronic alcohol consumption through a systematic and narrative review, with detailed descriptions of the occurrences. Methods. A systematic and narrative review of literature that evaluates noncommunicable diseases associated with chronic alcohol consumption was carried out using Google, Medline and databases of major international health organizations. Keywords used as search terms were alcoholism, chronic alcohol use and heavy alcohol use; these terms were matched with occurrences and risk of noncommunicable diseases. Studies included in this review are clinical trials, meta-analyses, randomized controlled trials, and systematic and review articles. Results. The findings revealed that chronic alcohol use is either a single or joint risk factor for Alzheimer’s disease and dementia, arthritis, brain malfunction, cancer (most commonly of the oropharynx, larynx, oesophagus, liver, colon, rectum or breast), chronic obstructive pulmonary disease (COPD), diabetes, epilepsy, heart diseases and cardiovascular diseases, immune system dysfunction, malnourishment and vitamin deficiencies, mood disorders, bipolar disorder and depression, osteoporosis and bone malformation, pancreatitis, and ulcers and gastrointestinal problems. Conclusion. These findings are background information as they revealed some of the noncommunicable diseases associated with chronic alcohol use. Hence, more and precise long-term cohort studies are necessary for a better understanding of the occurrences and epidemiology of noncommunicable diseases as a result of chronic alcohol use.

show abstract

“…As reported recently, the elevated Nrf2 activity can also be evoked by EPO-stimulated ERKs and PI3K/AKT pathways, and Nrf2 can mediate the neuroprotective effects of EPO (18–20). Nevertheless, although oxidative stress plays a critical role in chronic alcoholism-related injuries (21–23), whether Nrf2 activity is involved in the autonomous and non-autonomous repair of alcoholic brain damage remains elusive.…”

Section: Introductionmentioning

confidence: 99%

Intranasal erythropoietin ameliorates neurological function impairments and neural pathology in mice with chronic alcoholism by regulating autophagy‑related Nrf2 degradation

Nie

Wang

et al. 2018

Mol Med Report

View full text Add to dashboard Cite

The neurological disorders and neural pathology brought about by chronic alcoholism are difficult to be reversed. Increasing evidence highlights the protective roles of erythropoietin (EPO) in neurodegenerative diseases and injuries of the central nervous system. In the present study, we investigated the therapeutic effects of EPO on the neurological function deficits and neural pathology caused by chronic alcoholism and the regulatory mechanisms. Using the canonical mouse model of chronic alcohol exposure designed to mimic the repeated cycles of heavy abuse typical of chronic alcoholism, it was found that EPO delivered via intranasal route effectively restored the alcohol-impaired motor cooperation in rotarod and beam walk tests, reversed alcoholic cognitive and emotional alterations in the novel location recognition task and open-filed test, and rescued alcohol-disrupted nervous conduction in the somatosensory-evoked potential (SSEP) test. Consistently, the intranasally administered EPO promoted the remyelination and synapse formation in chronic alcohol-affected neocortex and hippocampus as evidenced by immunofluorescence staining and transmission electron microscopy. Additionally, we discovered that the exogenous rhEPO, which entered the cerebrum through intranasal route, activated the erythropoietin receptor (EPOR) and the downstream ERKs and PI3K/AKT signaling, and suppressed autophagy-related degradation of nuclear factor, erythroid 2-like 2 (Nrf2). Furthermore, the intranasal EPO-exerted neuroprotection was almost abolished when the specific Nrf2 antagonist ATRA was administered intraperitoneally prior to intranasal EPO treatment. Collectively, our data demonstrated the repairing potential of EPO for the neurological disorders and neural pathology caused by chronic alcoholism, and identified the Nrf2 activity as the key mechanism mediating the protective effects of EPO.

show abstract

Chronic Alcohol Ingestion and Predisposition to Lung “Cirrhosis”

Cited by 3 publications

References 23 publications

Adamts1 Mediates Ethanol‐Induced Alterations in Collagen and Elastin via a FoxO1‐Sestrin3‐AMPK Signaling Cascade in Myocytes

Adamts1 Mediates Ethanol‐Induced Alterations in Collagen and Elastin via a FoxO1‐Sestrin3‐AMPK Signaling Cascade in Myocytes

Chronic Alcohol Use and Accompanying Noncommunicable Diseases

Intranasal erythropoietin ameliorates neurological function impairments and neural pathology in mice with chronic alcoholism by regulating autophagy‑related Nrf2 degradation

Contact Info

Product

Resources

About