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Last update 08 May 2025

COL5A1

Last update 08 May 2025

Basic Info

Synonyms

COL5A1, Collagen alpha-1(V) chain, collagen type V alpha 1 chain

Introduction

Type V collagen is a member of group I collagen (fibrillar forming collagen). It is a minor connective tissue component of nearly ubiquitous distribution. Type V collagen binds to DNA, heparan sulfate, thrombospondin, heparin, and insulin.

Drugs associated with COL5A1

CCB-005

Target

COL5A1

Mechanism

COL5A1 inhibitors [+1]

Active Org.

Castle Creek Biosciences, Inc.

Originator Org.

Mayo Clinic

Active Indication

Ehlers-Danlos Syndrome

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with COL5A1

100 Translational Medicine associated with COL5A1

0 Patents (Medical) associated with COL5A1

644

Literatures (Medical) associated with COL5A1

09 Apr 2025·Science Translational Medicine

Collagen V regulates renal function after kidney injury and can be pharmacologically targeted to enhance kidney repair in mice

Article

Author: Deb, Arjun ; Hilser, James R. ; Pellegrini, Matteo ; Gu, Yiqian ; Zhang, Guanglin ; Li, Yusheng ; Pan, Calvin ; Espinoza, Alejandro ; Hanudel, Mark R. ; Sun, Qihao ; Zhang, Linlin ; Tao, Bo ; Alvarez, Juan Felipe ; Lusis, Aldons J. ; Hartiala, Jaana A. ; Allayee, Hooman ; Su, Lianjiu ; Li, Shen

Kidney fibrosis determines clinical outcomes in individuals with chronic kidney disease (CKD). The stoichiometric ratio of collagens in renal scar differs from that of healthy kidney extracellular matrix (ECM), but the functional importance of altered collagen types in injured kidneys remains unclear. Using human population studies, we show that circulating protein and renal mRNA amounts of collagen V A1 (COL5A1) exhibited associations with kidney disease and incident CKD risk. We show that Col5a1 regulates the degree of postinjury fibrosis and renal function. Mice with conditionally knocked out Col5a1 ( Col5a1 CKO) exhibited decreased renal function and greater renal fibrosis after dietary adenine- or ureteric obstruction–mediated kidney injury. Renal fibroblasts in Col5a1 CKO animals up-regulated the profibrotic αvβ3 integrin. Inhibition of αvβ3 signaling with a small molecule, cilengitide, rescued postinjury renal function in Col5a1 CKO animals. Using the hybrid mouse diversity panel that comprises 100 diverse inbred strains of mice, we observed that gene expression of Col5a1 after injury exhibited genetic variation across 100 strains. Strains with low Col5a1 expression after injury exhibited worse renal function compared with animals that had higher degrees of expression. We next measured Col5a1 expression in peripheral blood mononuclear cells in mice to identify nonresponder strains that did not have increased Col5a1 expression after kidney injury. We observed that administration of cilengitide in nonresponder strains significantly rescued postinjury renal fibrosis and function. These studies point to the feasibility of precision medicine approaches to target Col5a1 for enhancing renal repair.

03 Apr 2025·Current Eye Research

Expression of PAX6 and Keratocyte-Characteristic Markers in Human Limbal Stromal Cells of Congenital Aniridia and Healthy Subjects, In Vitro

Article

Author: Amini, Maryam ; Suiwal, Shweta ; Seitz, Berthold ; Zimmermann, Julia ; Shi, Lei ; Fries, Fabian N. ; Li, Zhen ; Stachon, Tanja ; Trusen, Simon ; Berger, Maximilian ; Chai, Ning ; Szentmáry, Nóra

PURPOSEOur aim was to examine the expression of PAX6 and keratocyte-specific markers in human limbal stromal cells (LSCs) in congenital aniridia (AN) and in healthy corneas, in vitro.METHODSPrimary human LSCs were extracted from individuals with aniridia (AN-LSCs) (n = 8) and from healthy corneas (LSCs) (n = 8). The cells were cultured in either normal-glucose serum-containing cell culture medium (NGSC-medium) or low-glucose serum-free cell culture medium (LGSF-medium). Analysis of PAX6 and keratocyte-specific markers was conducted using qPCR and Western blotting. The keratocyte-specific markers included Collagen I (COL1A1), Collagen III (COL3A1), Collagen V (COL5A1), α-smooth muscle actin (ACTA2), Aldehyde Dehydrogenase 3 Family, Member A1 (ALDH3A1), Keratocan (KER), Lumican (LUM), and CD34.RESULTSPAX6 mRNA expression exhibited a significant decrease in AN-LSCs compared to LSCs in both NGSC- and LGSF-medium (p = 0.04; p = 0.014). There was a marked reduction in COL5A1 mRNA expression (p = 0.011), accompanied by notably higher ALDH3A1 and KER mRNA levels (p = 0.007; p = 0.013) in AN-LSCs compared to LSCs when using NGSC-medium. In LGSF-medium, AN-LSCs showed a significant increase in COL1A1 and COL5A1 mRNA expression compared to LSCs (p = 0.048; p = 0.002). Moreover, COL1A1 and α-SMA protein expression were significantly elevated in AN-LSCs compared to LSCs in LGSF-medium (p = 0.048, p = 0.008).CONCLUSIONSOur investigation affirms the altered expression of PAX6 and keratocyte-specific markers in AN-LSCs relative to healthy controls. Both NGSC- and LGSF-medium exerted distinct effects on both LSCs and AN-LSCs. The observed variations in PAX6 and keratocyte-specific marker expression in AN-LSCs may play a pivotal role in the development and progression of aniridia-associated keratopathy.

01 Apr 2025·Cancer Reports

Predicting Prognosis and Immunotherapy Response in Glioblastoma (GBM) With a 5‐Gene CAF‐Risk Signature

Article

Author: Tong, Luqing ; Zhan, Renya ; He, Haifeng ; Shi, Rui ; Yan, Min ; Zhang, Shengxiang ; Ye, Ke ; Zhu, Yu

ABSTRACTBackgroundCancer‐associated fibroblasts (CAF) represent significant constituents within the extracellular matrix (ECM) across a range of cancers. Nevertheless, there exists a scarcity of direct proof concerning the function of CAF in glioblastoma (GBM).AimsThis study endeavors to probe the participation of CAF in GBM by developing and validating a CAF‐risk signature and exploring its correlation with immune infiltration and immunotherapy responsiveness.Methods and ResultsTo fulfill these objectives, mRNA expression profiles of GBM samples and their corresponding clinical data were retrieved from two databases. First, stromal CAF‐associated genes were identified by weighted gene co‐expression network analysis (WGCNA). This method constructs co‐expression networks and pinpoints gene modules with similar expression patterns to detect relevant genes. Subsequently, a CAF‐risk signature was established via univariate and LASSO Cox regression analyses. Thereafter, gene set enrichment analysis (GSEA) and single‐sample gene set enrichment analysis (ssGSEA) were carried out to investigate the underlying molecular mechanisms. The immune status was evaluated with several R packages, and the Tumor Immune Dysfunction and Exclusion (TIDE) algorithm was utilized to assess the response to immunotherapy. Validation was performed using single‐cell RNA sequencing (scRNA) datasets, the Cancer Cell Line Encyclopedia (CCLE), and the Human Protein Atlas (HPA). Eventually, a 5‐gene (ITGA5, MMP14, FN1, COL5A1, and COL6A1) prognostic CAF model was constructed. Notably, immune infiltration analysis demonstrated a significant correlation between Treg, Macrophage, and CAF risk scores. Moreover, TIDE analysis suggested a decreased responsiveness to immunotherapy in high CAF‐risk patients. In addition, GSEA showed significant enrichment of the transforming growth factor alpha (TGF‐α), inflammatory response, and epithelial–mesenchymal transition (EMT) pathways in this subgroup. Finally, the validation through scRNA, CCLE, and HPA datasets confirmed these findings.ConclusionThe 5‐gene CAF‐risk signature exhibited accurate prognostic predictions and efficiently evaluated clinical immunotherapy responses among GBM patients. These results offer robust evidence regarding the implication of CAF in GBM and underscore the potential clinical value of personalized anti‐CAF therapies in conjunction with immunotherapy.

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COL5A1

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