MicroRNA Dysregulation in NSAID/Stress-Induced Gastric Ulcers: Restoration of Mucosal Integrity via RNA- Mediated Healing by Phytochemicals (A narrative review)
), Abubakar M. Garba(2), Umar Z. Usman(3), Saidu Kasimu(4), Onwuchekwa Chinedu(5),
(1) Department of Physiology, Faculty of Basic Medical Sciences, College of Health Sciences, Prince Abubakar Audu University PMB, 1008, Anyigba, Kogi State, Nigeria. Department of Physiology, Faculty of Basic Medical Sciences, College of Health Sciences, Usmanu Danfodiyo University PMB, 2254, Sokoto, Sokoto State, Nigeria.
(2) Department of Physiology, Faculty of Basic Medical Sciences, College of Health Sciences, Prince Abubakar Audu University PMB, 1008, Anyigba, Kogi State, Nigeria.
(3) Department of Physiology, Faculty of Basic Medical Sciences, College of Health Sciences, Prince Abubakar Audu University PMB, 1008, Anyigba, Kogi State, Nigeria.
(4) Department of Chemical Pathology and Immunology, Faculty of Clinical Sciences, College of Health Sciences, Usmanu Danfodiyo University PMB, 2254, Sokoto, Sokoto State, Nigeria.
(5) Department of Physiology, Faculty of Basic Medical Sciences, College of Health Sciences, Prince Abubakar Audu University PMB, 1008, Anyigba, Kogi State, Nigeria.
Corresponding Author
Abstract
Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) and physiological stress remain leading causes of gastric ulceration worldwide, yet current therapies incompletely address upstream injury pathways. Mounting evidence suggests that microRNAs (miRNAs) play a crucial role in coordinating mucosal vulnerability and repair.
Objectives: This narrative review synthesizes empirical studies that interrogate miRNA dynamics across established models of indomethacin/aspirin injury and restraint-stress paradigms, with ethanol/HCl comparators which were mechanistically informative.
Methods: A narrative review was NSAIDs or sympathoadrenal ischemia with mucus failure (stress) are models of ulcerogenesis that causes cyclooxygenase-1 inhibition and atropine-sensitive gastric hypermotility, driving oxidative stress, inflammatory signaling, mitochondrial dysfunction, and apoptosis.
Results and Discussion: Recurrent miRNA signatures include up-regulation of proinflammatory/apoptotic miRNAs—particularly matured microRNAs (miR) such as miR-21, miR-155, miR-181, and miR-34a—and stress-responsive miR-143/miR-152 that suppress the cystine transporter xCT/SLC7A11, thereby weakening glutathionebased antioxidant defenses. In parallel, cytoprotective miRNAs such as miR-223 and angiogenesis-supporting miRNAs (e.g., miR-126) tend to decline, collectively repressing targets involved in barrier integrity, redox homeostasis (xCT), survival signaling (BCL2/BAX balance), and restitution/angiogenesis. Interventional data, spanning pharmacologic comparators and plant-derived agents such as ginger and curcumin extracts, suggest that effective gastroprotection correlates with normalization of ulcer-associated miRNAs alongside restoration of redox tone and dampening of NF-?B/iNOS/COX-2 axes.
Conclusion: Overall, miRNA dysregulation provides a unifying mechanistic layer in peptic ulcer pathogenesis and a promising therapeutic entry point. Priorities include standardized miRNA panels across models, causal perturbation with mimics/antagomirs, pharmacokinetic optimization of miRNA-active phytochemicals, and translational studies leveraging circulating miRNAs as biomarkers of injury and healing.Keywords
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