Evidence mapPaperPMID 41470786Full record

ReviewNutrients2025

Therapeutic Potentials of Phytochemicals in Pancreatitis: Targeting Calcium Signaling, Ferroptosis, microRNAs, and Inflammation with Drug-Likeness Evaluation.

Fatma Farhat, Balaji Venkataraman, Bhoomendra A Bhongade, Mauro Pessia, Shreesh Ojha, Sandeep B Subramanya

Abstract readReview
In one paragraph

Review in Nutrients, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Fatma FarhatDepartment of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain P.O. Box 15551, United Arab Emirates.ORCID 0000-0003-0289-8216
Balaji VenkataramanDepartment of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain P.O. Box 15551, United Arab Emirates.ORCID 0000-0001-6561-2399
Bhoomendra A BhongadeDepartment of Pharmaceutical Chemistry, RAK College of Pharmaceutical Chemistry, RAK Medical & Health Sciences University, Ras Al Khaimah P.O. Box 15551, United Arab Emirates.ORCID 0000-0002-4057-7125
Mauro PessiaDepartment of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain P.O. Box 15551, United Arab Emirates.ORCID 0000-0002-2857-6795
Shreesh OjhaDepartment of Pharmacology and Therapeutics, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain P.O. Box 15551, United Arab Emirates.ORCID 0000-0001-7801-2966
Sandeep B SubramanyaDepartment of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain P.O. Box 15551, United Arab Emirates.ORCID 0000-0002-4802-500X

Funding

United Arab Emirates University 12R169
6 · The paper itself

Abstract

backgroundPancreatitis, encompassing acute (AP), severe acute (SAP), and chronic (CP) forms, is a life-threatening inflammatory disorder with limited therapeutic options. Current management is largely supportive, highlighting the urgent need for novel interventions targeting underlying molecular pathways.

aimThis review summarizes recent advances in the pathogenesis of pancreatitis, focusing on calcium dysregulation, ferroptosis, and microRNA-mediated mechanisms while exploring the therapeutic potential of phytochemicals as disease-modifying agents. SUMMARY: Aberrant calcium signaling, iron-dependent lipid peroxidation, and microRNA imbalance drive acinar cell injury, inflammatory cascades, and pancreatic fibrosis. Phytochemicals, including flavonoids, terpenoids, alkaloids, and phenolics, have shown protective effects in preclinical models through multi-targeted mechanisms. These include suppression of NF-κB-driven inflammation, activation of the Nrf2/HO-1 antioxidant pathway, modulation of ferroptosis via GPX4 and iron efflux, regulation of calcium signaling, and modulation of microRNA expression. Importantly, several phytochemicals attenuate acinar cell death, reduce cytokine release, and limit fibrosis, thereby improving outcomes in experimental pancreatitis. However, poor solubility, bioavailability, and pharmacokinetic limitations remain significant barriers. Emerging strategies such as nanotechnology-based formulations, prodrug design, and pharmacokinetic profiling, as well as bioavailability studies, may enhance their clinical applicability.

conclusionsPhytochemicals represent a promising reservoir of multitarget therapeutic agents for pancreatitis. Their ability to modulate oxidative stress, inflammatory and calcium signaling, ferroptosis, and microRNA networks highlights their translational potential. Future studies should focus on clinical validation, bioavailability optimization, and advanced delivery platforms to bridge the gap from bench to bedside.

Indexed as

Calcium SignalingFerroptosisMicroRNAsPancreatitisPhytochemicalsAnimalsHumansInflammationMicroRNAsPhytochemicalsacute pancreatitiscalcium signalingchronic pancreatitisdrug-likenessferroptosismicroRNAsnanotechnologyNF-κBNrf2pancreatitisphytochemicals

Identifiers

PMID41470786
PMCPMC12735687

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.