Mitochondria-Targeted Therapies Show Promise for Acute Pancreatitis
- Authors
- Serge Chooklin, Serhii Chuklin
- Journal
- Digestive Diseases and Sciences
- Year
- 2026
- DOI
- 10.1007/s10620-026-09806-9
- Study Type
- clinical
- Peer Reviewed
- Yes
- Country
- Ukraine
- Health Condition
- Acute Pancreatitis
- Body System
- Digestive System
TL;DR
Scientists found that targeting the "power plants" inside pancreas cells (called mitochondria) could be a promising new way to treat severe pancreatic inflammation, because these damaged power plants are a big part of what makes pancreatitis so harmful. The catch is that while this approach works really well in lab tests and animal studies, doctors haven't yet proven it works in real patients, so more testing is needed before it can become an actual treatment.
Key Finding
Multiple mitochondria-targeted compounds reduced pancreatic injury in laboratory and animal models of acute pancreatitis, but clinical evidence in humans remains limited.
Summary
This review examined research on how targeting mitochondria (the energy-producing structures in cells) might help treat acute pancreatitis, a serious inflammation of the pancreas. Researchers looked at dozens of studies testing various compounds—including hydrogen-rich saline, coenzyme Q10, melatonin, and others—that aim to restore mitochondrial function and reduce pancreatic damage. Most evidence comes from laboratory and animal studies showing these approaches can work, but very few human trials have been conducted yet.
Practical Takeaway
While this review identifies hydrogen-rich saline and other mitochondrial-support compounds as promising in early research, the evidence is almost entirely from animal studies and lab work—not human trials. Anyone interested in these approaches should know that translation to actual clinical benefit in patients has not yet been established, and more rigorous human studies are needed before any health claims can be made.
Abstract
Purpose: To synthesize experimental and clinical evidence on mitochondria-targeted strategies in acute pancreatitis (AP) and evaluate the potential of interventions that preserve or restore mitochondrial function to reduce pancreatic injury and systemic complications. Methods: We conducted a narrative review of PubMed, Scopus, and Google Scholar through 2025, focusing on preclinical and clinical studies assessing mitochondrial structure/function or interventions targeting mitochondrial pathways in AP. Outcomes included mitochondrial membrane potential (ΔΨm), ATP content, mitochondrial reactive oxygen species (mtROS), mitochondrial permeability transition pore (mPTP) opening, calcium handling, mitophagy and biogenesis markers (e.g., PINK1/Parkin, PGC-1α/NRF1/TFAM), and cell death, with selective inclusion of early clinical data. Results: Multiple mitochondria-targeted strategies consistently mitigated pancreatic injury in cellular and animal models of AP. Bioenergetic support with L-carnitine, NAD+ precursors, coenzyme Q10, deoxyarbutin, and melatonin restored ATP levels and stabilized ΔΨm, while ΔΨm preservation and mPTP modulation by irisin, cyclosporine/NIM811, and TRO40303 limited necrosis. Redox modulation using Nrf2 activators (sulforaphane, paeonol, hydroxytyrosol, curcumin), MitoTEMPO, tiron, and hydrogen-rich saline reduced mtROS production and inflammasome activation, although MitoQ and SkQ1 showed mixed or adverse effects. Restraining pathological calcium flux through ruthenium red-mediated MCU inhibition prevented Ca2+-induced mitochondrial collapse, and enhancement of organelle quality control via rapamycin, urolithin A, selenium, and trehalose promoted mitophagy and mitochondrial biogenesis. Several interventions also attenuated extra-pancreatic organ injury. However, evidence remains predominantly preclinical, heterogeneous, and limited by challenges in targeted delivery across the hemato-pancreatic barrier. Conclusion: Mitochondria-targeted therapies offer a mechanistically grounded strategy to reduce AP severity. Key priorities include optimizing pharmacokinetics and targeting, harmonizing experimental and clinical endpoints, and conducting rigorously designed clinical trials to translate preclinical benefits into meaningful patient outcomes.