Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (747 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A group of compounds containing the porphin structure, four pyrrole rings connected by methine bridges in a cyclic configuration to which a variety of side chains are attached. The nature of the side chain is indicated by a prefix, as uroporphyrin, hematoporphyrin, etc. The porphyrins, in combination with iron, form the heme component in biologically significant compounds such as hemoglobin and myoglobin.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Porphyrin.
Where it fits in the MeSH classification
- Broader topics
- Tetrapyrroles; Pigments, Biological
- Narrower topics
- Coproporphyrins; Deuteroporphyrins; Etioporphyrins; Hematoporphyrins; Mesoporphyrins; Metalloporphyrins; Porphyrinogens; Protoporphyrins; Uroporphyrins; Verteporfin
- See also
- Porphobilinogen
Research landscape
PubMed indexes 53,514 records tagged with the MeSH heading “Porphyrins” (counts retrieved 2026-10-31). 7,378 of them (13.8%) were published from 2020 onward, and the busiest period so far is through 1999 with 21,161 records.
Reviews account for 3,562 records (6.7%) and meta-analyses for 40. Randomized controlled trials number 329 (0.6%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 21,161 |
| 2000-2009 | 12,377 |
| 2010-2019 | 12,598 |
| 2020 onward | 7,378 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 3,562 | 6.7% |
| Meta-analyses | 40 | 0.1% |
| Randomized controlled trials | 329 | 0.6% |
Method: PubMed query "Porphyrins"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| The role of heme in sepsis induced Kupffer cell PANoptosis and senescence | 2025 | Research article Design not recorded in structured metadata | 28 | cc by PMID 40221420 · DOI · PMC11993645 |
| Targeting G-quadruplex by TMPyP4 for inhibition of colorectal cancer through cell cycle arrest and boosting anti-tumor immunity | 2024 | Research article Design not recorded in structured metadata | 23 | cc by PMID 39528472 · DOI · PMC11554887 |
| Photodynamic gel-bombs enhance tumor penetration and downstream synergistic therapies | 2025 | Research article Design not recorded in structured metadata | 21 | cc by PMID 40102383 · DOI · PMC11920195 |
| Proteasome-guided haem signalling axis contributes to T cell exhaustion | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 41851457 · DOI · PMC13658038 |
The role of heme in sepsis induced Kupffer cell PANoptosis and senescence [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Elevated heme levels, a consequence of hemolysis, are strongly associated with increased susceptibility to bacterial infections and adverse sepsis outcomes, particularly in older populations.
- Closing excerpt
- These findings establish mitochondrial damage as a central mediator of heme induced Kupffer cell loss and highlight PLC-γ inhibition and hemopexin administration as promising therapeutic strategies for combating sepsis associated immune dysfunction.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (216 words)
Elevated heme levels, a consequence of hemolysis, are strongly associated with increased susceptibility to bacterial infections and adverse sepsis outcomes, particularly in older populations. However, the underlying mechanisms remain poorly understood. Using a cecal ligation and puncture (CLP) model of sepsis, we demonstrate that elevated heme levels correlate with Kupffer cell loss, increased bacterial burden, and heightened mortality. Mechanistically, we identify mitochondrial damage as a key driver of heme- and bacterial-induced Kupffer cell PANoptosis, a form of cell death integrating pyroptosis, apoptosis, and necroptosis, as well as cellular senescence. Specifically, heme activates phospholipase C gamma (PLC-γ), facilitating the translocation of cleaved gasdermin D (c-GSDMD) to mitochondria, resulting in GSDMD pore formation, mitochondrial dysfunction, and the release of mitochondrial DNA (mtDNA) during bacterial infection. This mitochondrial damage amplifies PANoptosis and triggers the cGAS-STING signaling pathway, further driving immune senescence. Notably, PLC-γ inhibition significantly reduces mitochondrial damage, cell death, and senescence caused by heme and bacterial infection. Furthermore, we show that hemopexin, a heme scavenger, effectively mitigates sepsis-induced Kupffer cell death and senescence, enhances bacterial clearance, and improves survival outcomes in both young and aged mice. These findings establish mitochondrial damage as a central mediator of heme induced Kupffer cell loss and highlight PLC-γ inhibition and hemopexin administration as promising therapeutic strategies for combating sepsis associated immune dysfunction.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40221420 · DOI · PMC11993645
Targeting G-quadruplex by TMPyP4 for inhibition of colorectal cancer through cell cycle arrest and boosting anti-tumor immunity [2]
Abstract reading summary — source excerpts
- Opening excerpt
- G-quadruplex (G4) is a noncanonical DNA secondary structure known to induce DNA damage and regulate the expression of immune-related genes.
- Closing excerpt
- In summary, our findings underscore the potential of the G4 ligand TMPyP4 as a dual strategy to target colorectal cancer: inhibiting cancer progression and augmenting anti-tumor immunity through the activation of cGAS-STING pathway.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (173 words)
G-quadruplex (G4) is a noncanonical DNA secondary structure known to induce DNA damage and regulate the expression of immune-related genes. We aim to exploit the G4 folding as a treatment strategy to trigger anti-tumor immune response. In this study, we observe that the abundant genomic G4 in epithelial cells coexists with increased infiltration of CD8+ T cells in colorectal cancer tissue. Furthermore, our data substantiate the inhibitory effect of the G4 ligand TMPyP4 on cancer progression while concurrently stimulating anti-tumor immunity. Mechanistically, TMPyP4 impedes cancer cell proliferation and induces G2/M cell cycle arrest. Additionally, in vivo experiments demonstrate that TMPyP4 enhances the anti-tumor immune response by triggering DNA damage and activating the cGAS-STING pathway, which fosters CD8+ T cell activation and dendritic cell maturation. Importantly, the combined treatment of TMPyP4 and anti-PD1 exhibits a synergistic therapeutic effect on colorectal cancer. In summary, our findings underscore the potential of the G4 ligand TMPyP4 as a dual strategy to target colorectal cancer: inhibiting cancer progression and augmenting anti-tumor immunity through the activation of cGAS-STING pathway.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39528472 · DOI · PMC11554887
Photodynamic gel-bombs enhance tumor penetration and downstream synergistic therapies [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Nanoparticle-based drug delivery system remains a significant challenge in the current treatment of solid tumors, primarily due to their limited penetration capabilities.
- Closing excerpt
- As expected, the enhanced penetration and accumulation of therapeutic components into tumor tissues can be achieved, significantly enhancing the anti-proliferation capacity against breast cancer.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (183 words)
Nanoparticle-based drug delivery system remains a significant challenge in the current treatment of solid tumors, primarily due to their limited penetration capabilities. Herein, we successfully engineer photodynamic gel-bombs (DCM@OPR) capable of penetrating deeply into tumor tissues utilizing the photodynamic-triggered explosive energy and receptor-mediated transcytosis, significantly enhancing the therapeutic efficacy of breast cancer. The photodynamic gel-bombs were fabricated by loading powerful components of chlorin e6 and MnO2 nanoparticles, as well as Doxorubicin, into a crosslinked Ca2+-gel. Upon exposure to laser irradiation, the obtained photodynamic gel-bombs are capable of generating explosive energy, resulting in their fragmentation into numerous nanofragments. The photodynamic-triggered explosive energy subsequently drives these nanofragments to deeply penetrate into tumor tissues through gap leakage among tumor cells. In addition, the photodynamic-triggered explosive energy also promotes the escape of those therapeutic components (including chlorin e6, MnO2 nanoparticles, and doxorubicin) and nanofragments from lysosomes. In the subsequent stages, these nanofragments also exhibit excellent transcytosis capacity, facilitating deep penetration into tumor tissues. As expected, the enhanced penetration and accumulation of therapeutic components into tumor tissues can be achieved, significantly enhancing the anti-proliferation capacity against breast cancer.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40102383 · DOI · PMC11920195
Proteasome-guided haem signalling axis contributes to T cell exhaustion [4]
Abstract reading summary — source excerpts
- Opening excerpt
- The accumulation of depolarized mitochondria commits T cells to exhaustion1-3, yet the precise mechanism remains unclear.
- Closing excerpt
- Our findings identify a proteasome-guided haem signalling axis, governed by mitochondrial integrity, as a regulator of CD8+ T cell exhaustion and propose innovative therapeutic strategies that exploit this pathway to optimize adoptive cellular immunotherapy.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (175 words)
The accumulation of depolarized mitochondria commits T cells to exhaustion1-3, yet the precise mechanism remains unclear. Here we find that exhausted CD8+ T cells increase proteasome activity owing to the accumulation of depolarized mitochondria, which drives the selective degradation of mitochondrial proteins and the release of regulatory haem through haemoprotein breakdown. In turn, increased regulatory haem disrupts BACH2-mediated transcriptional regulation, thereby exacerbating T cell exhaustion and compromising stemness-like properties. Inhibition of nuclear import of regulatory haem prevents BACH2 degradation and enhances the anti-tumour efficacy of antigen-specific T cells. We find that the therapeutic efficacy of human CD19+ chimeric antigen receptor (CAR)-T cells in patients with B cell acute lymphoblastic leukaemia negatively correlates with the proteasome gene signature in their CAR-T cells. Manufacturing CAR-T cells in the presence of bortezomib, an FDA-approved proteasome inhibitor, prevents T cell exhaustion and improves therapeutic efficacy. Our findings identify a proteasome-guided haem signalling axis, governed by mitochondrial integrity, as a regulator of CD8+ T cell exhaustion and propose innovative therapeutic strategies that exploit this pathway to optimize adoptive cellular immunotherapy.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41851457 · DOI · PMC13658038
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Oxygen Activation and Radical Transformations in Heme Proteins and Metalloporphyrins [5]
- Research article Macrophages and Iron Metabolism [6]
- Research article Porphyrins at interfaces [7]
- Research article Porphyrin-Based Metal-Organic Frameworks for Biomedical Applications [8]
- Research article Glycosylated Porphyrins, Phthalocyanines, and Other Porphyrinoids for Diagnostics and Therapeutics [9]
- Research article Prokaryotic Heme Biosynthesis: Multiple Pathways to a Common Essential Product [10]
References
- Li T, Adams J, Zhu P, Zhang T, Tu F, Gravitte A, et al.. The role of heme in sepsis induced Kupffer cell PANoptosis and senescence. . 2025. PMID 40221420 · DOI · PMC11993645
- Li P, Zhou D, Xie Y, Yuan Z, Huang M, Xu G, et al.. Targeting G-quadruplex by TMPyP4 for inhibition of colorectal cancer through cell cycle arrest and boosting anti-tumor immunity. . 2024. PMID 39528472 · DOI · PMC11554887
- Bai X, Meng F, Wang X, He L, Fan C, Tian L, et al.. Photodynamic gel-bombs enhance tumor penetration and downstream synergistic therapies. . 2025. PMID 40102383 · DOI · PMC11920195
- Xu Y, Shangguan Y, Chuang YM, Chang TH, Liu W, Peng JJ, et al.. Proteasome-guided haem signalling axis contributes to T cell exhaustion. . 2026. PMID 41851457 · DOI · PMC13658038
- Huang X, Groves JT. Oxygen Activation and Radical Transformations in Heme Proteins and Metalloporphyrins. Chem Rev. 2018. PMID 29286645 · DOI · PMC5855008
- Soares MP, Hamza I. Macrophages and Iron Metabolism. Immunity. 2016. PMID 26982356 · DOI · PMC4794998
- Auwärter W, Écija D, Klappenberger F, Barth JV. Porphyrins at interfaces. Nat Chem. 2015. PMID 25615664 · DOI
- Chen J, Zhu Y, Kaskel S. Porphyrin-Based Metal-Organic Frameworks for Biomedical Applications. Angew Chem Int Ed Engl. 2021. PMID 31989749 · DOI · PMC7984248
- Singh S, Aggarwal A, Bhupathiraju NV, Arianna G, Tiwari K, Drain CM. Glycosylated Porphyrins, Phthalocyanines, and Other Porphyrinoids for Diagnostics and Therapeutics. Chem Rev. 2015. PMID 26317756 · DOI · PMC6011754
- Dailey HA, Dailey TA, Gerdes S, Jahn D, Jahn M, O'Brian MR, et al.. Prokaryotic Heme Biosynthesis: Multiple Pathways to a Common Essential Product. Microbiol Mol Biol Rev. 2017. PMID 28123057 · DOI · PMC5312243
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.