Ultimately, reducing or delaying these risk factors of aging may provide neuroprotection and delay the onset of disease progression
The destructive factors include stomach hydrochloric acid (HCl), mucosal hypoperfusion, free oxygen radicals, ethanol, Helicobacter pylori and excessive ingestion of non-steroidal anti-inflammatory drugs (NSAIDs) that promote the gastric mucosal injury and contribute to gastric ulceration [3]
In ALD, ethanol metabolism via hepatocyte CYP2E1 generates excess ROS and acetaldehyde, inducing endoplasmic reticulum stress and mitochondrial dysfunction [365]
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