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ABSTRACT
Introduction
Chronic pancreatitis (CP) is a persistent, recurrent, and progressive disorder that is characterized by chronic inflammation and irreversible fibrosis of the pancreas. It is associated with severe morbidity, resulting in intense abdominal pain, diabetes, exocrine and endocrine dysfunction, and an increased risk of pancreatic cancer. The etiological factors are diverse and the major risk factors include smoking, chronic alcoholism, as well as other environmental and genetic factors. The treatment and management of CP is challenging, and no definitive curative therapy is currently available.
Areas covered
This review paper aims to provide an overview of the different cell types in the pancreas that is known to mediate disease progression and outline potential novel therapeutic approaches and drug targets that may be effective in treating and managing CP. The information presented in this review was obtained by conducting a NCBI PubMed database search, using relevant keywords.
Expert opinion
In recent years, there has been an increased interest in the development of novel therapeutics for CP. A collaborative multi-disciplinary approach coupled with a consistent funding for research can expedite progress of translating the findings from bench to bedside.
Article highlights
Chronic pancreatitis is a fibro-inflammatory disease of the pancreas that has no targeted drug therapy till date due to its complex etiology.
Pancreatic stellate cells (PSCs) and macrophages primarily govern the pathobiology of chronic pancreatitis independently and by cross-talking.
Cell signaling pathways targeting activation of PSCs as well as macrophage-mediated inflammation and fibrosis could be of potential therapeutic benefit against chronic pancreatitis.
Research utilizing multiple study models of CP are required to counteract the complex etiology of chronic pancreatic injury.
Abbreviations
| AA | = | Arachidonic Acid |
| ADM | = | Acinar-To-Ductal Metaplasia |
| AMPKs | = | Adenosine Monophosphate Activated Protein Kinase |
| AP | = | Acute Pancreatitis |
| BMDMs | = | Bone Marrow-Derived Macrophages |
| BMPRs | = | Bone Morphogenetic Protein Receptors |
| BMPs | = | Bone Morphogenetic Proteins |
| CDE | = | Choline-deficient, ethionine-supplemented diet |
| Cox | = | Cyclooxygenases |
| CP | = | Chronic Pancreatitis |
| ECM | = | Extracellular Matrix |
| ERCP | = | Endoscopic Retrograde Cholangiopancreatography |
| FGF | = | Fibroblast Growth Factor |
| GLP-1 | = | Glucagon-Like Peptide 1 |
| GMCSF | = | Granulocyte-Macrophage Colony – Stimulating Factor |
| HO-1 | = | Hemoxygenase-1 |
| IFNγ | = | Interferon Gamma |
| IL | = | Interleukin |
| ILG | = | Isoliquiritigenin |
| iNOS | = | Inducible Nitric Oxide Synthase |
| KLF4 | = | Kruppel-Like Factor 4 |
| LPS | = | Lipopolysaccharide |
| MCP-1 | = | Monocyte Chemoattractant Protein − 1 |
| miR | = | Micro RNA |
| MMPs | = | Matrix Metalloproteases |
| Nrf2 | = | Nuclear Factor E2-Related Factor-2 |
| NSAIDs | = | Non-Steroidal Anti-Inflammatory Drug |
| PDGF | = | Platelet Derived Growth Factor |
| PERT | = | Pancreatic Enzyme Replacement Therapy |
| PSCs | = | Pancreatic Stellate Cells |
| RA | = | Retinoic Acid |
| RAP | = | Recurrent Acute Pancreatitis |
| RARs | = | Retinoic Acid Receptors |
| ROS | = | Reactive Oxygen Species |
| SIRT1 | = | Sirtuin 1 |
| STAT5A | = | Signal Transducer And Activator Of Transcription 5A |
| TGFβ | = | Transforming Growth Factor – Beta |
| TIMPs | = | Tissue Inhibitor Of Matrix Metalloproteases |
| TNBS | = | Trinitrobenzenesulfonic Acid |
| TNFα | = | Tumor Necrosis Factor – Alpha |
| TP53INP1 | = | Tumor Protein P53- Induced Nuclear Protein 1 |
| YN | = | Yttrium Oxide Nanoparticles |
| αSMA | = | Alpha-Smooth Muscle Actin |
Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.