Liver inflammation

Liver inflammation is not a molecule or receptor but a complex biological process characterized by the infiltration of immune cells—particularly macrophages, natural killer (NK) cells, and various T cell subsets—into the liver tissue in response to infectious, metabolic, autoimmune, toxic, or other forms of injury[1][2][3]. This multifaceted response is mediated by the release of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), and often involves changes in cellular metabolism, cell death pathways, and fibrogenesis. Chronic liver inflammation plays a central role in the progression to liver fibrosis, cirrhosis, and hepatocellular carcinoma[4][5]. In clinical and research contexts, numerous molecules are targeted to modulate this process (e.g., signaling pathways of NF-κB, JNK, TGF-β, and immune cell interactions), but "liver inflammation" itself is not a discrete protein, gene, or conventional drug target, making it unsuitable as a canonical molecular target[1][4][5][7]. Note: - "Liver inflammation" should not be listed as a therapeutic molecular target—such as a receptor, enzyme, transporter, or transcription factor—but rather as a *pathological process or category* involving multiple, specific molecular targets[1][2][4]. - Relevant research and interventions focus on molecular mediators (e.g., cytokines, immune receptors, signaling molecules) that drive or modulate hepatic inflammation.

Other names

Liver inflammation