ArticleInternational journal of colorectal disease2024
PKG1 promotes the HIV-induced proliferation, migration, and fibrosis of vascular smooth muscle cells of hemorrhoids.
Article in International journal of colorectal disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Role of HIV-encoded proteins in cardiovascular disease.American journal of physiology. Cell physiology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
backgroundHemorrhoids are very common in patients with human immunodeficiency virus (HIV) infection. The risk of postoperative infection is significantly greater in HIV-positive patients than in HIV-negative individuals, and the wound healing time is significantly prolonged. This study aimed to investigate the role of HIV-associated hemorrhoids from the perspective of vascular smooth muscle cell (VSMC) function.
methodsA total of 24 hemorrhoid tissue samples (note: grade IV hemorrhoids were absence) were collected and subjected to Masson staining to evaluate fibrosis in this study. mRNA and protein levels were monitored by qPCR and WB analysis, respectively. Immunofluorescence was conducted to evaluate PKG1 and α-SMA expression. To establish a cell model in vitro, VSMCs were stimulated with envelope glycoprotein (gp) 120, which is a type of HIV envelope protein. Cell proliferation was assessed via a CCK-8 assay and EdU staining. Moreover, a wound healing assay was performed to assess cell migration.
resultsOur data confirmed that fibrosis was present in hemorrhoid tissues from HIV-infected patients and that PKG1 expression was upregulated. Moreover, the administration of HIV gp120 promoted the proliferation and migration of VSMCs. Similarly, fibrosis-related markers (α-SMA, MMP2, MMP3, and TIMP1) were markedly upregulated. However, silencing PKG1 inhibited the proliferation, migration, and expression of fibrosis-related markers in gp120-challenged VSMCs.
conclusionThe present research revealed that PKG1 regulated the proliferation, migration, and fibrosis of VSMCs, thereby exerting detrimental effects on HIV-associated hemorrhoids.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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 OpenQuestion graph.