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Immune Genes as Markers for the Management of Prolonged Hepatic Damage
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Opinion Article - American Journal of Physiology, Biochemistry and Pharmacology (2024)

Immune Genes as Markers for the Management of Prolonged Hepatic Damage

Safavi Gwen*
 
Department of Pharmacology, Gyalpozhing College of Information Technology, Mongar, Bhutan
 
*Corresponding Author:

Safavi Gwen, Department of Pharmacology, Gyalpozhing College of Information Technology, Mongar, Bhutan, Email: gwen_safavi09@gamil.com

Received: 26-Dec-2023, Manuscript No. AJPBP-24-126581; Editor assigned: 29-Dec-2023, Pre QC No. AJPBP-24-126581 (PQ); Reviewed: 12-Jan-2024, QC No. AJPBP-24-126581 ; Revised: 19-Jan-2024, Manuscript No. AJPBP-24-126581 (R); Published: 26-Jan-2024

Description

Chronic hepatic injury, a condition characterized by prolonged inflammation and damage to the liver, poses a significant global health burden. The intricate interplay between the immune system and hepatic cells plays a crucial role in the development and progression of chronic liver diseases. Recent advancements in genomics have opened new avenues for understanding the underlying immune mechanisms and predicting potential drugs to mitigate chronic hepatic injury. This article discusses about the exploration of immune genes and their role in predicting drugs for the treatment of chronic hepatic injury [1].

The complex landscape of chronic hepatic injury

Chronic hepatic injury encompasses a spectrum of liver diseases, including chronic hepatitis, cirrhosis, and hepatocellular carcinoma. The liver, a vital organ with multifaceted functions, is susceptible to various insults, such as viral infections, alcohol abuse, and metabolic disorders. The immune system, comprising innate and adaptive components, actively participates in the liver’s response to injury. Immune cells, cytokines, and chemokines orchestrate a complex network that can either promote tissue repair or lead to chronic inflammation and fibrosis [2,3].

Understanding immune genes in chronic hepatic injury

Genomic studies have shed light on the role of immune genes in the context of chronic hepatic injury. Researchers have identified specific genes associated with immune response modulation, inflammation, and fibrogenesis. These genes, when deregulated, contribute to the persistence of liver damage and the progression of chronic liver diseases.

Cytokines and chemokines

Cytokines and chemokines are key mediators of immune responses in the liver. Certain immune genes encode these signalling molecules, influencing the recruitment and activation of immune cells. Interleukins, Tumour Necrosis Factor-Alpha (TNF-α), and Transforming Growth Factor-Beta (TGF-β) are examples of cytokines implicated in chronic liver diseases [4].

Immune cells and receptors

Genes associated with immune cell function, such as macrophages, T cells, and natural killer cells, play a crucial role in the liver’s response to injury. The expression levels of receptors like Toll-like receptors (TLRs) and Pattern Recognition Receptors (PRRs) influence the recognition of pathogens and subsequent immune activation [5,6].

Fibrogenesis and extracellular matrix remodelling

Chronic hepatic injury often leads to fibrosis, a process characterized by excessive extracellular matrix deposition. Genes involved in fibrogenesis, such as collagen genes and Matrix Metallo- Proteinases (MMPs), contribute to the structural changes in the liver associated with chronic liver diseases [7].

Predicting potential drugs through immune genomics

Advancements in genomic technologies have paved the way for precision medicine approaches in treating chronic hepatic injury. By analyzing the immune gene landscape, researchers can identify potential drug targets and develop personalized therapeutic strategies. Several approaches have been employed to predict drugs for the treatment of chronic liver diseases.

Genome-Wide Association Studies (GWAS): GWAS analyze genetic variations across individuals to identify associations with specific diseases. In the context of chronic hepatic injury, GWAS have revealed candidate genes that may serve as targets for drug development. Polymorphisms in certain immune genes have been linked to susceptibility or resistance to liver diseases.

Expression profiling and transcriptomics: Transcriptomic analysis allows researchers to study gene expression patterns in response to chronic hepatic injury. By identifying up regulated or down regulated immune genes, potential drug targets can be pinpointed. This approach provides insights into the dynamic changes in the immune response during the progression of liver diseases [8].

Pharmacogenomics: Pharmacogenomics explores how genetic variations influence an individual’s response to drugs. Understanding the genetic basis of drug metabolism and efficacy in the context of chronic hepatic injury can guide the selection of appropriate therapies. This personalized approach aims to maximize treatment efficacy while minimizing adverse effects [9].

Network analysis: Integrating data from various sources, including genomics, proteomics, and metabolomics, allows for a comprehensive understanding of the molecular networks involved in chronic hepatic injury. Network analysis helps identify key nodes or hubs that could be targeted by drugs to modulate the immune response and mitigate liver damage.

The integration of immune genomics into the study of chronic hepatic injury has opened up exciting possibilities for predicting potential drugs and advancing personalized therapeutic interventions. The complex interplay between immune genes and the progression of liver diseases provides a rich landscape for exploration. As research in this field continues to evolve, the identification of precise drug targets and the development of tailored treatment strategies hold the promise of improving outcomes for individuals with chronic hepatic injury. By unravelling the intricate genetic and immunological mechanisms at play, researchers pave the way for a future where liver diseases are not only better understood but also effectively treated through targeted and personalized approaches [10].

References