Bacterial Toxins: A Hope Towards Angiogenic Ailments

Rekha Khandia, Khandia R, Ashok Munjal, Munjal A, Kuldeep Dhama, Dhama K, Yashpal Singh Malik, Malik YS
Current drug metabolism · 2017 · doi:10.2174/1389200218666170911150948 · PMID:28901253
review OA: closed public-domain-us
Full text JSON View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-08-10 ⓘ

This review elucidates how bacterial toxins can modulate angiogenesis by mimicking or competing with pro-angiogenic factors, potentially serving as therapeutics for angiogenic disorders.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by qwen3.7-flash, 2026-09-08 · read from full text ⓘ

This review article synthesizes existing literature to explore how bacterial toxins can modulate angiogenesis, a process critical in both excessive and reduced vascular growth. The authors explain that these toxins function by mimicking pro-angiogenic factors, competing with them, or altering receptor activity through mechanisms involving Rho signaling and GTPases. While the paper highlights the potential of bacterial toxins as novel therapeutics for various disorders, it focuses primarily on the molecular mechanisms rather than clinical trial data. Relevance to endometriosis: listed as one indication for anti-angiogenic approaches, though the paper's main focus is on the general therapeutic potential of bacterial toxins across multiple diseases.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

BACKGROUND: Angiogenesis is an essential physiological process for growth and maintenance of the body. Especially its role becomes indispendable during the embryonic development stage but lacks in adults with some exceptions like while wound repair and menstrual cycle. It is a tightly regulated process and relies on the cascade of several molecular signaling pathways with the involvement of many effectors like vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), insulin-like growth factor (IGF) etc. METHODS: Related literature/ information were retrieved, analyzed and compiled from the online published resources available in Medline, Pubmed, Pubmed Central, Science Direct and other scientific databases. RESULTS: Excessive angiogenesis leads to disorders like tumor, atherosclerosis, rheumatoid arthritis, diabetic retinopathy, endometriosis, psoriasis, and adiposity. While, reduced angiogenesis also results in several ailments like cardiac ischemia, low capillary density in brain of Alzheimer's patients and delayed wound healing. Therefore, both angio-proliferative and anti-angiogenic approaches may be of use in developing novel therapeutics. Bacterial toxins are known for modulating the process of angiogenesis by mimicking pro-angiogenic factors and/ or competing with them. Furthermore, they inactivate the receptors or keep them in ON status, hence can be used to treat angiogenic disorders. The ease in handling, cultivation and manipulating the toxins structure has enabled the use of bacteria as an ideal choice for novel therapeutic developments. CONCLUSION: This review intends to elucidate the molecular mechanisms through which certain bacteria may alter the level of angiogenesis and consequently can work as therapeutics against angiogenic disorders.
Full text 1,421 characters · extracted from oa-doi-fallback · 4 sections · click to expand

Abstract

Methods: Related literature/ information were retrieved, analyzed and compiled from the online published resources available in Medline, Pubmed, Pubmed Central, Science Direct and other scientific databases.

Results

Excessive angiogenesis leads to disorders like tumor, atherosclerosis, rheumatoid arthritis, diabetic retinopathy, endometriosis, psoriasis, and adiposity. While, reduced angiogenesis also results in several ailments like cardiac ischemia, low capillary density in brain of Alzheimer's patients and delayed wound healing. Therefore, both angio-proliferative and anti-angiogenic approaches may be of use in developing novel therapeutics. Bacterial toxins are known for modulating the process of angiogenesis by mimicking pro-angiogenic factors and/ or competing with them. Furthermore, they inactivate the receptors or keep them in ON status, hence can be used to treat angiogenic disorders. The ease in handling, cultivation and manipulating the toxins structure has enabled the use of bacteria as an ideal choice for novel therapeutic developments.

Conclusion

This review intends to elucidate the molecular mechanisms through which certain bacteria may alter the level of angiogenesis and consequently can work as therapeutics against angiogenic disorders.

Keywords

Angiogenesis, bacterial toxins, Rho signaling, GTPases, endothelial cells, stress fibres, actin bundles, apoptosis inhibition.

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

⚙ Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback ⓘ

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Condition tags

endometriosis

MeSH descriptors

Angiogenesis Inhibitors Bacterial Toxins Neovascularization, Pathologic Angiogenesis Inhibitors Angiogenesis Inhibitors Animals Bacterial Toxins Bacterial Toxins Humans Neovascularization, Pathologic Neovascularization, Pathologic

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. The paper's references may be in our DB but unresolved to ``paper_id`` (resolution happens at ingest when the cited DOI matches a row we already have). Run the cross-source citation reconcile pass to retry.

Source provenance

europepmc
last seen: 2026-09-17T06:16:55.786923+00:00
pubmed
last seen: 2026-05-13T22:20:13.663096+00:00
unpaywall
last seen: 2026-09-17T06:32:46.214484+00:00
License: public-domain-us · commercial use OK · attribution required
Courtesy of the U.S. National Library of Medicine