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. 2026 Feb 13;105(7):e47637. doi: 10.1097/MD.0000000000047637

Aldehyde reductase as potential measurement for retinitis pigmentosa: A two-sample Mendelian randomization (MR) study

Weiming Yan a,*, Pan Long b, Chengming Chen a, Xiaohong Zhang a, Tao Chen c
PMCID: PMC12908768  PMID: 41686564

Abstract

This study aimed to utilize Mendelian randomization (MR) analysis to investigate potential genetic targets related to aldehyde metabolism in the context of retinitis pigmentosa (RP) and to identify possible therapeutic options. Genome-wide association study data for RP were obtained for MR analysis. We employed various statistical methods, including inverse-variance weighted analysis, to evaluate potential causal associations with RP risk, followed by rigorous sensitivity analysis. Two-sample MR analysis identified a significant causal relationship between aflatoxin B1 (AFB1) aldehyde reductase and the risk of RP, with genetically predicted AFB1 aldehyde reductase contributing to a decreased risk of RP (odds ratio: 0.875; P = .008) based on inverse-variance weighted analysis. Sensitivity analysis suggested no evidence of heterogeneity or horizontal pleiotropy in the observed associations (P > .05). Additionally, the leave-one-out validation confirmed the robustness of these findings without significant alterations. The results from the reverse analysis for the causal relationship between the accidence of RP and AFB1 aldehyde reductase showed no significant statistical differences. Our findings highlighted the role of AFB1 aldehyde reductase in the pathogenesis of RP, proposing it as a promising protective measure for future treatment strategies.

Keywords: aflatoxin B1 aldehyde reductase, aldehyde, bioinformatics, Mendelian, retinitis pigmentosa

1. Introduction

Retinitis pigmentosa (RP) encompasses a diverse group of inherited retinal dystrophies that primarily affect the photoreceptor cells within the retina, leading to progressive vision loss.[1] Characterized by night blindness, loss of peripheral vision, and eventual central vision impairment, RP affects millions worldwide and significantly impacts the quality of life for affected individuals. The genetic basis of RP is complex, involving mutations in over 60 different genes, which complicates the understanding of its pathophysiology and presents challenges for effective therapeutic interventions.[2] Recent advances in genetic research and molecular biology have begun to illuminate the intricate pathways involved in RP, offering insights that could inform the development of targeted therapies.[3] Among these pathways, aldehyde metabolism has emerged as a key area of interest in retinal diseases.[4] Aldehyde reductase is an important enzyme in this metabolic process, responsible for catalyzing the reduction of various aldehydes, including potentially toxic compounds that may accumulate in retinal cells.[5] The enzyme’s role in detoxifying aldehydes suggests that it may be protective against oxidative stress and inflammation, both of which are implicated in the degeneration of photoreceptor cells. Evidence from previous studies indicated that aldehyde metabolism might plays a significant role in RP. Chen et al demonstrated that retinoid dehydrogenases RDH8 and RDH12 were crucial for reducing all-trans-retinal in photoreceptors, with RDH12 protecting cells from aldehyde toxicity.[6] Daich Varela et al highlighted the role of RDH12 in clearing toxic aldehydes, with mutations in RDH12 linked to RP and other retinal dystrophies.[7] Zigler et al proposed that lipid peroxidation products, including toxic aldehydes, contributed to lens damage in retinal degenerative diseases like RP.[8] Similarly, Choudhary et al found that retinal pigment epithelial cells detoxified aldehydes like HNE, and their accumulation might contribute to retinal degeneration, a condition of retinal pigment epithelial cells damage related to RP.[9]

Mendelian randomization (MR) is a powerful statistical approach that leverages genetic variants as instrumental variables (IVs) to infer causal relationships between exposures and outcomes.[10] This method helps mitigate confounding variables and reverse causation biases that can obscure true associations in observational studies. By utilizing the two-sample MR, researchers can analyze the effects of an exposure (in this case, aldehyde reductase activity) on an outcome (the risk of developing RP) using separate datasets. This approach not only enhances the reliability of the findings but also allows for the integration of large-scale genomic data.[11] In this study, we aimed to explore the potential causal relationship between aflatoxin B1 (AFB1) aldehyde reductase activity and the risk of developing RP through a two-sample MR analysis. By leveraging existing genome-wide association study (GWAS) data,[12] we tried to clarify whether enhancing the activity of aldehyde reductase could serve as a protective factor against the progression of RP. Our findings could have significant implications for the development of novel therapeutic strategies aimed at preserving retinal function and improving outcomes for individuals affected by this debilitating condition.

2. Materials and methods

2.1. MR data sources and study design

We conducted a two-sample MR analysis, a robust statistical technique that leverages genetic variants as IVs to infer causal relationships between exposures and outcomes. This study design allowed us to explore the potential causal impact of AFB1 aldehyde reductase activity on the risk of developing RP using distinct datasets for exposure and outcome, thus minimizing biases associated with confounding variables and reverse causation that often plagued observational studies. Since this study utilized publicly available summary statistics and did not involve direct participant data, ethical approval was not required. However, all included datasets were derived from studies that had obtained appropriate ethical clearances from their respective institutional review boards. In addition, our work adhered to the STROBE-MR guidelines (https://www.strobe-mr.org/) for reporting MRs (Fig. 1).

Figure 1.

Figure 1.

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Flowchart of the Mendelian randomization (MR) analysis of the causal effect of aldehyde reductase on retinitis pigmentosa (RP) in our study. Genetic instruments for aldehyde reductase were selected from the IEU OpenGWAS with the threshold to satisfy the 3 core assumptions: relevance, exclusion restriction, and independence. Analysis were performed in both directions, with the inverse-variance weighted (IVW) method used as the primary approach for estimating the exposure–outcome relationship. GWAS = genome-wide association study, IVW = inverse-variance weighted, MR = Mendelian randomization, RP = retinitis pigmentosa.

2.2. Data collection

Our study utilized publicly available GWAS data from the IEU OpenGWAS Project (https://gwas.mrcieu.ac.uk/) to investigate the relationship between genetic susceptibility to aldehyde reductase and the risk of RP. Permissions were obtained to access the GWAS database, as it is a utilized publicly available summary statistics. We applied keywords of RP and aldehydes to extract data from the GWAS resources. The accessible information on the GWAS sources, the phenotypic code, for the selected data were prot-c-4188_1_2 and ebi-a-GCST90013904. The link to the resources used for this analysis were https://gwas.mrcieu.ac.uk/datasets/prot-c-4188_1_2/ and https://gwas.mrcieu.ac.uk/datasets/ebi-a-GCST90013904/ (Table 1).

Table 1.

Overview of the data sources used in our MR study of the causality of retinitis pigmentosa (RP).

Phenotypes Data source Phenotypic code Sample size Number of SNPs Ancestry
Exposures
 Aflatoxin B1 aldehyde reductase Suhre K prot-c-4188_1_2 – 5,01,428 European
Outcomes
 RP Ben Elsworth ebi-a-GCST90013904 4,03,833 1,10,38,457 European
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MR = Mendelian randomization, RP = retinitis pigmentosa, SNP = single-nucleotide polymorphism.

GWAS data for RP

To identify genetic variants associated with RP, we utilized summary statistics from large-scale GWAS. These databases typically included thousands of RP cases and matched controls, providing a rich resource for understanding the genetic architecture of the disease. We focused on studies with significant findings that met the stringent genome-wide significance threshold (P < 5 × 10−8), ensuring that the selected variants had robust associations with RP risk. Summary-level data for RP involved 4,03,833 individuals with 1,10,38,457 single nucleotide polymorphisms (SNPs; the sample size, n = 1,10,38,457).

AFB1 aldehyde reductase data

For the exposure data, we sought out SNPs that were significantly associated with AFB1 aldehyde reductase activity. We ensured that the selected SNPs were functionally relevant and had demonstrated associations with the enzyme’s activity in previous studies, thereby increasing the reliability of our IVs. In details, the data for AFB1 aldehyde reductase were extracted from a GWAS comprising a total of 5,01,428 SNPs (the sample size, n = 5,01,428).

2.3. Statistical analysis

The statistical analysis was performed in several steps to ensure the robustness and validity of our findings:

SNPs selection

We identified a set of SNPs that were significantly associated with AFB1 aldehyde reductase based on established criteria. The selection process involved rigorous screening for linkage disequilibrium (LD) to ensure independence among selected SNPs. We retained only those variants with the highest associations to maintain statistical power in our analysis. Genetic variants (SNPs) were used as IVs to explore the causal relationship, following the 3 main assumptions in MR analysis: IVs are strongly related to exposure factors; IVs are not associated with confounding factors; and IVs only influence the risk of outcomes through exposure. In greater details, SNPs were chosen as IVs based on the genome-wide significance criterion (P < 5 × 10−8). To ensure the independence of these IVs, a LD threshold of r2 < 0.001 and a maximum genetic distance of 10,000 kb for SNPs grouping were set. The PhenoScanner tool was applied to examine the associations of each selected SNP with potential confounders. SNPs that showed significant associations with confounders, such as Vitamin A intake, light exposure, and known genetic factors like Pde6b, were excluded from the analysis. Furthermore, an F statistic threshold >10 was applied to select the final set of SNPs.

Causal estimation

For univariable analysis, we employed the inverse-variance weighted (IVW), MR-Egger, weighted median methods, and other approaches. The primary estimation method utilized was IVW, providing an asymptotic estimate of the standard error of the causal estimate from each variant. We employed IVW analysis to calculate the causal odds ratio (OR) that quantified the relationship between genetically predicted AFB1 aldehyde reductase activity and the risk of RP. The IVW method aggregated estimates from multiple SNPs, weighted by their variance, to produce a single summary estimate. This approach was particularly useful in MR studies, as it allowed for the incorporation of multiple genetic variants simultaneously. A two-sided P value < .05 was considered suggestive of significance. Sensitivity analysis: To ensure the robustness of our causal inference, we conducted several sensitivity analysis. These included: Heterogeneity tests: We assessed the heterogeneity among the SNPs included in the analysis to determine if they were consistent in their effect on RP risk. It was performed using Cochran’s Q statistic, where a non-significant result would indicate homogeneity across the estimates. Horizontal pleiotropy checks: We utilized methods such as the Egger regression and the weighted median estimator to detect and account for potential horizontal pleiotropy, which occured when SNPs influenced the outcome through pathways unrelated to the exposure of interest. Leave-one-out analysis: This involved systematically removing each SNP from the analysis to evaluate its individual impact on the overall results. This technique helped identify any outlier SNPs that could disproportionately influence the causal estimates. Software procession: All statistical analyses were performed using R version 4.1.0 (R Foundation for Statistical Computing Austria, https://www.r-project.org/). A two-sided P value < .05 was considered statistically significant.

3. Results

3.1. MR analysis on the causality of retinitis pigmentosa (RP)

In our MR analysis, we explored the causal relationship between genetic susceptibility of AFB1 aldehyde reductase activity and the risk of RP. We identified the SNPs associated with AFB1 aldehyde reductase activity as IVs that met the significance threshold. These variants were selected from large-scale GWAS data and were shown to be significantly linked to RP. In details, the identified SNPs included in our study were rs4364907, rs2215496, rs10861741, rs6661421, and rs9567824, respectively. Through the analysis of these SNPs with IVW method, we estimated the causal relationship between genetically predicted AFB1 aldehyde reductase activity and the risk of developing RP. The analysis yielded a mean OR of 0.875; (P = .008; 95% confidence interval [CI]: 0.787, 0.965), indicating that higher activity of the enzyme was associated with a decrease in the risk of RP. A significant association between AFB1 aldehyde reductase activity and the risk of RP was also identified by the weighted median analysis method (P = .045). No significant associations were observed using other statistical models such as MR-Egger, and MR-PRESSO (Fig. 2). In addition, the forestplot for each SNP and the combined effect in the MR analysis by the IVW also confirmed the significant association between AFB1 aldehyde reductase activity and the risk of RP (Fig. 3).

Figure 2.

Figure 2.

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The forestplot for the genetically prediction from Mendelian randomization analysis of the causal effect of aflatoxin B1 aldehyde reductase activity on the risk of RP. The inverse-variance weighted (IVW) method and the weighted median approach both revealed a significant association between aflatoxin B1 aldehyde reductase activity and the risk of RP. The odds ratio (OR) was <1, indicating a negative association. Red arrowhead: a statistical significance was detected. CI = confidence interval, IVW = inverse-variance weighted, nSNP = numbers of single-nucleotide polymorphism, OR = odd ratio, RP = retinitis pigmentosa.

Figure 3.

Figure 3.

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The forestplot for each SNP and the combined effect in the Mendelian randomization analysis of aflatoxin B1 aldehyde reductase activity on the risk of RP: focusing on each SNP and the overall effect. The combined effect of SNPs from the IVW method confirmed a significant association between aflatoxin B1 aldehyde reductase activity and the risk of RP. IVW = inverse-variance weighted, RP = retinitis pigmentosa, SNP = single-nucleotide polymorphism.

In addition, the scatterplot of MR analysis revealed the linear slopes of the effect of each AFB1 aldehyde reductase activity-associated genetic variant on RP on the log-odds scale, especially by the IVW method. In addition, we did not observe that the intercepts of the all the analysis methods deviated from zero in all studies, demonstrating that there was no horizontal pleiotropy (Fig. 4).

Figure 4.

Figure 4.

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The scatterplot of MR analysis on the causality between genetic susceptibility to aflatoxin B1 aldehyde reductase activity and the risk of RP. The scatterplot demonstrated the effect of each aflatoxin B1 aldehyde reductase activity-associated genetic variant on RP on the log-odds scale. The slopes of each line represented the causal association for each method, with a downward slope indicating a negative correlation. The intercepts of all analysis methods deviated from 0 across all studies, suggesting the absence of horizontal pleiotropy. MR = Mendelian randomization, RP = retinitis pigmentosa, SNP = single-nucleotide polymorphism.

For the MR sensitivity analysis, there was no evidence of heterogeneity in the associations between the causality between genetic susceptibility to AFB1 aldehyde reductase activity and the risk of RP in the Cochrane Q analysis (IVW: P = .466). In addition, no horizontal pleiotropy for the MR analysis was found in the association between genetic susceptibility to AFB1 aldehyde reductase activity and the risk of RP in the MR-Egger analysis (P = .619; Table 2).

Table 2.

Heterogeneity and pleiotropy tests for the associations between the causality between genetic susceptibility to aflatoxin B1 aldehyde reductase activity and the risk of RP.

MR analysis SNPs Heterogeneity tests (inverse variance weighted) Pleiotropy tests
Q Q_df Q_Pval Egger_intercept SE P
Aflatoxin B1 aldehyde reductase activity-RP 43 3.578 43 .466 0.047 0.086 .619
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MR = Mendelian randomization, RP = retinitis pigmentosa, SNPs = single-nucleotide polymorphisms.

Furthermore, the leave-one-out validation analysis examining the causal effect of AFB1 aldehyde reductase activity on the risk of RP demonstrated that the error line did not exhibit a statistically significant difference after removing each SNP individually (Fig. 5). Additionally, the funnelplot of our study displayed a relatively symmetric distribution, suggesting an overall stability in the SNPs and no significant bias during their selection for studying the causal effect of AFB1 aldehyde reductase activity on the risk of RP (Fig. 6).

Figure 5.

Figure 5.

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The leave-one-out plots and sensitivity analysis of MR analysis on the causality between genetic susceptibility to aflatoxin B1 aldehyde reductase activity and the risk of RP. The error line did not show a statistically significant difference after removing each SNP individually, further supporting the causal relationship between genetic susceptibility to aflatoxin B1 aldehyde reductase activity and the risk of RP. MR = Mendelian randomization, RP = retinitis pigmentosa, SNP = single-nucleotide polymorphism.

Figure 6.

Figure 6.

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The funnelplot of MR analysis on the causality between genetic susceptibility to aflatoxin B1 aldehyde reductase activity and the risk of RP. Each point represented a SNP in the funnelplot of our study. The symmetry distributionof the graph indicated overall stability, suggesting no significant bias in the selection of SNPs for studying the causal effect of aflatoxin B1 aldehyde reductase activity on the risk of RP. MR = Mendelian randomization, RP = retinitis pigmentosa, SNP = single-nucleotide polymorphism.

In the other direction across all MR analysis methods, we found no evidence of statistical significance in the causal relationship of RP with AFB1 aldehyde reductase activity (IVW: OR: 0.852; 95% CI: 0.609, 1.191, P = .348; Fig. 7). The corresponding MR sensitivity analysis showed no evidence of heterogeneity and horizontal pleiotropy in the association between RP and AFB1 aldehyde reductase activity (Cochrane Q: 1.143, P = .565; MR-Egger: −0.129, P = .581; Table 3). The leave-one-out validation analysis did not reveal any changes in the statistical difference after taking out each SNP in the analysis for the casual effect of RP on AFB1 aldehyde reductase activity (Fig. 8).

Figure 7.

Figure 7.

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The forestplot for the genetical prediction from Mendelian randomization analysis of the causal effect of RP on aflatoxin B1 aldehyde reductase activity. The IVW method of MR analysis revealed no statistical significance in the causal relationship between RP and aflatoxin B1 aldehyde reductase activity, as the error line crossed the zero point. CI = confidence interval, IVW = inverse-variance weighted, MR = Mendelian randomization, nSNP = numbers of single-nucleotide polymorphism, OR = odd ratio, RP = retinitis pigmentosa.

Table 3.

Heterogeneity and pleiotropy tests for the association between RP and aflatoxin B1 aldehyde reductase activity.

MR analysis SNPs Heterogeneity tests (inverse variance weighted) Pleiotropy tests
Q Q_df Q_Pval Egger_intercept SE P
RP-Aflatoxin B1 aldehyde reductase activity 3 1.143 242 .565 −0.129 0.167 .581
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MR = Mendelian randomization, RP = retinitis pigmentosa, SNP = numbers of single-nucleotide polymorphism.

Figure 8.

Figure 8.

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The leave-one-out plots of the MR analysis on the casual effect of RP on aflatoxin B1 aldehyde reductase activity. After removing each SNP individually, the error line still did not revealed a statistical significance in the causal relationship between RP and aflatoxin B1 aldehyde reductase activity. MR = Mendelian randomization, RP = retinitis pigmentosa, SNP = single-nucleotide polymorphism.

4. Discussion

Our analysis provided a compelling evidence of a causal relationship between AFB1 aldehyde reductase activity and the risk of RP. The consistent findings across various sensitivity analysis enhanced our confidence in this association. These results suggested that metabolic pathways involving AFB1 aldehyde reductase may play a significant role in the development of RP conditions, warranting further investigation into the underlying biological mechanisms.

In details, the SNPs identified in our study include rs4364907, rs2215496, rs10861741, rs6661421, and rs9567824. These SNPs were further anaylzed through a search of the NCBI dbSNP database (https://www.ncbi.nlm.nih.gov/snp/), which contains information on human single nucleotide variations, microsatellites, small-scale insertions and deletions, as well as publication data, population frequencies, molecular consequences, and genomic and RefSeq mappings for both common variants and clinical mutations. The rs2215496 was located on chromosome 17 and was reported to be in moderate LD associated with high-density lipoprotein cholesterol in a previous study.[13] This region may be relevant to multiple phenotypes, particularly those associated with lipid metabolism. Additionally, this SNP was nearby NLRP1 and might play a role in binding motifs, and in methylating histones. The rs10861741, located on chromosome 12, was reported to be associated with pigmentation traits, particularly human hair color and skin pigmentation. Besides, significant univariate associations have been observed in BTBD11, a gene previously shown to be associated with hair color in European populations.[14,15] In the context of RP in our study, the aforementioned SNPs may also be implicated in retinal pigment epithelium function as well as in lipid and aldehyde metabolism, although further investigations were required to elucidate their precise biological roles. The remaining 3 SNPs – rs4364907, rs6661421, and rs9567824 – were located on chromosomes 1 and 13, respectively. To date, no detailed functional studies have been reported regarding their potential biological relevance or involvement in disease pathogenesis.

With the above identified SNPs, we applied the two-sample MR approaches and revealed a negative association between AFB1 aldehyde reductase activity and RP. The main estimation method used in our study was IVW, an asymptotic estimate of the standard error of the causal estimate from each variant.[16] Besides, we found no significant relationship between RP and AFB1 aldehyde reductase activity on the other side. All our results of MR analysis suggested that higher AFB1 aldehyde reductase activity may decrease the risk of developing RP, which was aligned with previous literatures suggesting a possible involvement of the aldehyde metabolic component in the RP disease’s etiology.[17,18] Besides, these genetic variants, by influencing biochemical pathways related to AFB1 metabolism, might alter retinal function and susceptibility to RP.

AFB1, a potent mycotoxin, is primarily recognized for its carcinogenic properties, predominantly affecting the liver.[19] AFB1 contains an aldehyde group (−CHO) in its molecular structure, which is located on the aromatic ring. This aldehyde group is a critical component of its chemical reactivity and plays a significant role in its toxicity. Its metabolic byproducts, such as AFB1 aldehyde, may contribute to oxidative stress and cellular damage. AFB1 undergoes metabolic conversion in the body, where aldehyde reductases, particularly AFB1 aldehyde reductase, are involved in detoxifying its reactive metabolites.[20,21] AFB1 aldehyde reductase, encoded by the AKR7A2 gene, is part of the aldo-keto reductase (AKR) superfamily. cDNA clones encoding human AFB1 aldehyde reductase have been expressed in Escherichia coli, and the recombinant enzymes have been purified from E. coli for further study.[22] These enzymes play a role in reducing the accumulation of toxic aldehydes, which may contribute to oxidative stress and cellular damage. Research by Bodreddigari et al suggested that AFB1 aldehyde reductase metabolized AFB1 to reduce cytotoxicity, with findings indicating protection against AFB1-induced cytotoxicity through the expression of cloned AFB1-aldehyde reductases.[23]

Oxidative stress is a well-documented factor in various retinal diseases, including RP.[24] In the context of RP, oxidative stress is a key contributor to the degeneration of photoreceptor cells. The accumulation of toxic aldehydes could exacerbate the status of oxidative stress, further damaging the retina and leading to the progressive vision loss characteristic of RP.[25,26] Research by Ellis et al suggested that AFB1 aldehyde reductase could regulate oxidative stress-related genes. Specifically, the expression of this enzyme was significantly increased in rat liver by cancer chemopreventive agents, many of which were believed to regulate gene expression through the antioxidant response element.[27] Thus, the potential mechanism through which AFB1 influenced RP may involve the accumulation of reactive oxygen species, leading to photoreceptor cell degeneration. Furthermore, the involvement of AFB1 aldehyde reductase in detoxifying reactive metabolites suggested that its increased activity might not only serve as a compensatory response to reduce AFB1 levels but also helped protect the retina from cumulative oxidative damage. This implicit role could alter disease progression or offer potential therapeutic benefits. Despite the strength of our findings, there were limitations in our study. Firstly, in terms of MR analysis, our screening scope was relatively limited. We were unable to analyze all aldehydes target genes. The reliance on genetic data for causality assumeed that the selected SNPs were valid instruments without pleiotropic effects. Although our sensitivity analysis supported this assumption, the possibility of unmeasured confoundings could not be entirely ruled out. Another limitation of our study was the relatively small number of SNPs extracted. Although a statistically significant association was observed, the strength of this association and its potential for generalization may be constrained. Additionally, the generalizability of our findings could be limited due to the lack of demographic data from a population-based study.

In conclusion, our study contributed to the growing body of evidence linking aldehydes metabolic processes to the inherited retinal degenerative diseases, RP. By establishing a causal relationship between AFB1 aldehyde reductase activity and RP risk, we provided a foundation for further exploration into the interplay between genetics, metabolism, and environmental factors in the pathogenesis of this challenging condition. Further functional studies are necessary to explore the biological mechanisms underlying these associations and their role in retinal degeneration. Moreover, the associated SNPs could potentially serve as biomarkers for predicting RP risk in individuals with altered aldehyde reductase activity. Continued research in this area could have the potential to unveil novel therapeutic strategies for RP.

Author contributions

Conceptualization: Weiming Yan.

Data curation: Weiming Yan, Pan Long, Chengming Chen, Xiaohong Zhang, Tao Chen.

Formal analysis: Pan Long, Chengming Chen, Xiaohong Zhang, Tao Chen.

Funding acquisition: Tao Chen.

Investigation: Pan Long, Tao Chen.

Methodology: Tao Chen.

Supervision: Weiming Yan.

Writing – original draft: Weiming Yan.

Writing – review & editing: Weiming Yan, Pan Long, Tao Chen.

Abbreviations:

AFB1
aflatoxin B1
CI
confidence interval
GWAS
genome-wide association study
IV
instrumental variable
IVW
inverse-variance weighted
LD
linkage disequilibrium
MR
Mendelian randomization
OR
odds ratio
RP
retinitis pigmentosa
SNP
single nucleotide polymorphism

This work was supported by the grants from the National Natural Science Foundation of China (No. 82301245), the Natural Science Foundation of Fujian Province, China (No. 2024J011148), the Joint Funds for the innovation of science and Technology, Fujian province (No. 2024Y9653), and the Postdoctoral Science Foundation of the Fuzhou General Hospital (Grant number: 48678).

All the authors agreed the publication of this article.

Ethics approval was not required since this study utilized publicly available summary statistics and did not involve direct participant data.

The authors have no conflicts of interest to disclose.

The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.

How to cite this article: Yan W, Long P, Chen C, Zhang X, Chen T. Aldehyde reductase as potential measurement for retinitis pigmentosa: A two-sample Mendelian randomization (MR) study. Medicine 2026;105:7(e47637).

Contributor Information

Pan Long, Email: panlong@163.com.

Chengming Chen, Email: chentao112022@126.com.

Xiaohong Zhang, Email: zhangxh22@126.com.

Tao Chen, Email: chentao112022@126.com.

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