Metabolic Reprogramming in Organ Fibrosis and Regeneration

Dear Colleagues,

Organ fibrosis and regeneration represent divergent yet interconnected outcomes of tissue injury. Fibrosis, driven by persistent damage and maladaptive repair, underlies the progression of chronic diseases affecting the liver, lung, kidney, heart, and other organs. In contrast, regenerative responses restore tissue architecture and function through the coordinated activation of parenchymal, stromal, and immune programs. A fundamental challenge in the field is to understand why similar injury signals culminate in irreversible fibrotic scarring in some contexts, while enabling effective regeneration in others.

Increasing evidence suggests metabolic reprogramming as a critical determinant of these outcomes. Cellular metabolism extends beyond bioenergetics to actively govern cell fate decisions, signaling networks, and epigenetic states. Injury-induced shifts in glucose, lipid, amino acid, and mitochondrial metabolism control the activation, persistence, and plasticity of fibrogenic cells. At the same time, regenerative repair requires tightly regulated metabolic adaptations to support cell proliferation and differentiation. Metabolic states also shape immune cell phenotypes and stromal–parenchymal communication, thereby influencing whether inflammation resolves or progresses toward chronic fibrosis.

Fibrotic tissues constitute metabolically altered microenvironments which drive metabolic adaptations that reinforce fibrogenic signaling and extracellular matrix production while constraining regenerative capacity. Although individual metabolic pathways have been linked to fibrosis and repair, critical gaps remain in understanding how metabolic rewiring integrates with transcriptional, epigenetic, mechanical, and immune programs across organs and disease stages.

This Special Issue aims to advance our understanding of how metabolic reprogramming governs organ fibrosis and regeneration. We invite original research, reviews, and perspectives that will shape this rapidly evolving area to stimulate conceptual advances and inform new strategies to limit fibrosis and promote functional regeneration.

Dr. Melanie Tran
Dr. Dong Yang
Guest Editors

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