loading page

Exploring the Theranostic roles of miRNA and Epigenetics in Autoimmune Diseases - A Comprehensive Review
  • +13
  • Sagnik Nag,
  • Oishi Mitra,
  • Garima Tripathi,
  • Souvik Samanta,
  • Bikramjit Bhattacharya,
  • Priti Chandane,
  • Sourav Mohanto,
  • Vino Sundararajan,
  • Sumira Malik,
  • Sarvesh Rustagi,
  • Suraj Adhikari,
  • Aroop Mohanty,
  • Darwin A. León‐Figueroa,
  • Alfonso J. Rodriguez-Morales,
  • Joshuan Barboza,
  • Ranjit Sah
Sagnik Nag
Vellore Institute of Technology
Author Profile
Oishi Mitra
Vellore Institute of Technology
Author Profile
Garima Tripathi
Vellore Institute of Technology
Author Profile
Souvik Samanta
Vellore Institute of Technology
Author Profile
Bikramjit Bhattacharya
Vellore Institute of Technology
Author Profile
Priti Chandane
University of Hyderabad
Author Profile
Sourav Mohanto
Yenepoya (Deemed to be University)
Author Profile
Vino Sundararajan
Vellore Institute of Technology
Author Profile
Sumira Malik
Amity University Jharkhand Campus
Author Profile
Sarvesh Rustagi
Uttaranchal University
Author Profile
Suraj Adhikari
Manipal College of Medical Sciences
Author Profile
Aroop Mohanty
AIIMS Gorakhpur
Author Profile
Darwin A. León‐Figueroa
Universidad de San Martín de Porres Facultad de Medicina Humana
Author Profile
Alfonso J. Rodriguez-Morales
Fundacion Universitaria Autonoma de las Americas
Author Profile
Joshuan Barboza
Universidad César Vallejo
Author Profile
Ranjit Sah
Tribhuvan University

Corresponding Author:[email protected]

Author Profile

Abstract

Autoimmune diseases (AD) are severe pathophysiological ailments that are stimulated by an exaggerated immunogenic response towards self-antigens, which can cause systemic or site-specific organ damage. An array of complex genetic and epigenetic facets majorly contributes to the progression of AD, thus providing significant insight into the regulatory mechanism of microRNA (miRNA). miRNAs are short, non-coding RNAs that have been identified as essential contributors to the post-transcriptional regulation of host genome expression and as crucial regulators of a myriad of biological processes such as immune homeostasis, T helper cell differentiation, central and peripheral tolerance, and immune cell development. Pertaining to the differential expression of miRNA attributed in target tissues and cellular bodies of innate and adaptive immunity, a paradigm of scientific expeditions suggests an optimistic correlation between immunogenic dysfunction and miRNA alterations. Therefore, it is not astonishing that dysregulations in miRNA expression patterns are now recognized in a wide spectrum of disorders, establishing themselves as potential biomarkers and therapeutic targets. Owing to its theranostic potencies, miRNA targets have been widely utilized in the development of biosensors and other therapeutic molecules originating from the same. This article tends to deliberate and conceptualize the brief pathogenesis and pertinent epigenetic regulatory mechanism as well as miRNA networks majorly affecting five different ADs namely Rheumatoid Arthritis (RA), Diabetes, Multiple Sclerosis (MS), Systemic Lupus Erythematosus (SLE) and Inflammatory Bowel Disorder (IBD) thereby providing novel theranostic interventions.
12 Apr 2023Submitted to Immunity, Inflammation and Disease
29 Apr 2023Submission Checks Completed
29 Apr 2023Assigned to Editor
26 Jun 2023Review(s) Completed, Editorial Evaluation Pending
04 Jul 2023Reviewer(s) Assigned
30 Aug 2023Editorial Decision: Revise Minor
26 Sep 20231st Revision Received
04 Oct 2023Submission Checks Completed
04 Oct 2023Assigned to Editor
04 Oct 2023Review(s) Completed, Editorial Evaluation Pending
04 Oct 2023Reviewer(s) Assigned
31 Oct 2023Editorial Decision: Revise Major
06 Nov 20232nd Revision Received
06 Nov 2023Assigned to Editor
06 Nov 2023Submission Checks Completed
06 Nov 2023Review(s) Completed, Editorial Evaluation Pending
09 Nov 2023Reviewer(s) Assigned
22 Nov 2023Editorial Decision: Accept
Dec 2023Published in Immunity, Inflammation and Disease volume 11 issue 12. https://doi.org/10.1002/iid3.1121