Introduction – Company Background

GuangXin Industrial Co., Ltd. is a specialized manufacturer dedicated to the development and production of high-quality insoles.

With a strong foundation in material science and footwear ergonomics, we serve as a trusted partner for global brands seeking reliable insole solutions that combine comfort, functionality, and design.

With years of experience in insole production and OEM/ODM services, GuangXin has successfully supported a wide range of clients across various industries—including sportswear, health & wellness, orthopedic care, and daily footwear.

From initial prototyping to mass production, we provide comprehensive support tailored to each client’s market and application needs.

At GuangXin, we are committed to quality, innovation, and sustainable development. Every insole we produce reflects our dedication to precision craftsmanship, forward-thinking design, and ESG-driven practices.

By integrating eco-friendly materials, clean production processes, and responsible sourcing, we help our partners meet both market demand and environmental goals.

Core Strengths in Insole Manufacturing

At GuangXin Industrial, our core strength lies in our deep expertise and versatility in insole and pillow manufacturing. We specialize in working with a wide range of materials, including PU (polyurethane), natural latex, and advanced graphene composites, to develop insoles and pillows that meet diverse performance, comfort, and health-support needs.

Whether it's cushioning, support, breathability, or antibacterial function, we tailor material selection to the exact requirements of each project-whether for foot wellness or ergonomic sleep products.

We provide end-to-end manufacturing capabilities under one roof—covering every stage from material sourcing and foaming, to precision molding, lamination, cutting, sewing, and strict quality control. This full-process control not only ensures product consistency and durability, but also allows for faster lead times and better customization flexibility.

With our flexible production capacity, we accommodate both small batch custom orders and high-volume mass production with equal efficiency. Whether you're a startup launching your first insole or pillow line, or a global brand scaling up to meet market demand, GuangXin is equipped to deliver reliable OEM/ODM solutions that grow with your business.

Customization & OEM/ODM Flexibility

GuangXin offers exceptional flexibility in customization and OEM/ODM services, empowering our partners to create insole products that truly align with their brand identity and target market. We develop insoles tailored to specific foot shapes, end-user needs, and regional market preferences, ensuring optimal fit and functionality.

Our team supports comprehensive branding solutions, including logo printing, custom packaging, and product integration support for marketing campaigns. Whether you're launching a new product line or upgrading an existing one, we help your vision come to life with attention to detail and consistent brand presentation.

With fast prototyping services and efficient lead times, GuangXin helps reduce your time-to-market and respond quickly to evolving trends or seasonal demands. From concept to final production, we offer agile support that keeps you ahead of the competition.

Quality Assurance & Certifications

Quality is at the heart of everything we do. GuangXin implements a rigorous quality control system at every stage of production—ensuring that each insole meets the highest standards of consistency, comfort, and durability.

We provide a variety of in-house and third-party testing options, including antibacterial performance, odor control, durability testing, and eco-safety verification, to meet the specific needs of our clients and markets.

Our products are fully compliant with international safety and environmental standards, such as REACH, RoHS, and other applicable export regulations. This ensures seamless entry into global markets while supporting your ESG and product safety commitments.

ESG-Oriented Sustainable Production

At GuangXin Industrial, we are committed to integrating ESG (Environmental, Social, and Governance) values into every step of our manufacturing process. We actively pursue eco-conscious practices by utilizing eco-friendly materials and adopting low-carbon production methods to reduce environmental impact.

To support circular economy goals, we offer recycled and upcycled material options, including innovative applications such as recycled glass and repurposed LCD panel glass. These materials are processed using advanced techniques to retain performance while reducing waste—contributing to a more sustainable supply chain.

We also work closely with our partners to support their ESG compliance and sustainability reporting needs, providing documentation, traceability, and material data upon request. Whether you're aiming to meet corporate sustainability targets or align with global green regulations, GuangXin is your trusted manufacturing ally in building a better, greener future.

Let’s Build Your Next Insole Success Together

Looking for a reliable insole manufacturing partner that understands customization, quality, and flexibility? GuangXin Industrial Co., Ltd. specializes in high-performance insole production, offering tailored solutions for brands across the globe. Whether you're launching a new insole collection or expanding your existing product line, we provide OEM/ODM services built around your unique design and performance goals.

From small-batch custom orders to full-scale mass production, our flexible insole manufacturing capabilities adapt to your business needs. With expertise in PU, latex, and graphene insole materials, we turn ideas into functional, comfortable, and market-ready insoles that deliver value.

Contact us today to discuss your next insole project. Let GuangXin help you create custom insoles that stand out, perform better, and reflect your brand’s commitment to comfort, quality, and sustainability.

🔗 Learn more or get in touch:
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Pillow OEM for wellness brands Vietnam

Are you looking for a trusted and experienced manufacturing partner that can bring your comfort-focused product ideas to life? GuangXin Industrial Co., Ltd. is your ideal OEM/ODM supplier, specializing in insole production, pillow manufacturing, and advanced graphene product design.

With decades of experience in insole OEM/ODM, we provide full-service manufacturing—from PU and latex to cutting-edge graphene-infused insoles—customized to meet your performance, support, and breathability requirements. Our production process is vertically integrated, covering everything from material sourcing and foaming to molding, cutting, and strict quality control.High-performance graphene insole OEM Taiwan

Beyond insoles, GuangXin also offers pillow OEM/ODM services with a focus on ergonomic comfort and functional innovation. Whether you need memory foam, latex, or smart material integration for neck and sleep support, we deliver tailor-made solutions that reflect your brand’s values.

We are especially proud to lead the way in ESG-driven insole development. Through the use of recycled materials—such as repurposed LCD glass—and low-carbon production processes, we help our partners meet sustainability goals without compromising product quality. Our ESG insole solutions are designed not only for comfort but also for compliance with global environmental standards.Thailand custom neck pillow ODM

At GuangXin, we don’t just manufacture products—we create long-term value for your brand. Whether you're developing your first product line or scaling up globally, our flexible production capabilities and collaborative approach will help you go further, faster.Cushion insole OEM manufacturing facility Taiwan

📩 Contact us today to learn how our insole OEM, pillow ODM, and graphene product design services can elevate your product offering—while aligning with the sustainability expectations of modern consumers.Taiwan OEM factory for footwear and bedding solutions

A Northwestern Medicine study challenges conventional beliefs about Parkinson’s disease. Previously, the degeneration of dopaminergic neurons was thought to trigger the disease. This new research suggests that the real instigators are dysfunctions in the neuron’s synapses, which occur even before neuronal degradation. Such findings emphasize the need for therapies targeting the synapses before the disease’s neuronal effects manifest. Damage starts much earlier than the death of dopamine neurons, scientists report. How two sisters’ misfortune led to discovery Findings open a new avenue for therapies Drugs need to target neuron synapses before neurons degenerate A groundbreaking new Northwestern Medicine study challenges a common belief in what triggers Parkinson’s disease. Degeneration of dopaminergic neurons is widely accepted as the first event that leads to Parkinson’s. However, the new study suggests that a dysfunction in the neuron’s synapses — the tiny gap across which a neuron can send an impulse to another neuron — leads to deficits in dopamine and precedes the neurodegeneration. Parkinson’s disease affects 1% to 2% of the population and is characterized by resting tremor, rigidity, and bradykinesia (slowness of movement). These motor symptoms are due to the progressive loss of dopaminergic neurons in the midbrain. A Shift in Therapeutic Strategies The findings, which were published on September 15 in the journal Neuron, open a new avenue for therapies, the scientists said. “We showed that dopaminergic synapses become dysfunctional before neuronal death occurs,” said lead author Dr. Dimitri Krainc, chair of neurology at Northwestern University Feinberg School of Medicine and director of the Simpson Querrey Center for Neurogenetics. “Based on these findings, we hypothesize that targeting dysfunctional synapses before the neurons are degenerated may represent a better therapeutic strategy.” The study investigated patient-derived midbrain neurons, which is critical because mouse and human dopamine neurons have a different physiology and findings in the mouse neurons are not translatable to humans, as highlighted in Krainc’s research recently published in Science. Dysfunctional Synapses in Genetic Parkinson’s Northwestern scientists found that dopaminergic synapses are not functioning correctly in various genetic forms of Parkinson’s disease. This work, together with other recent studies by Krainc’s lab, addresses one of the major gaps in the field: how different genes linked to Parkinson’s lead to degeneration of human dopaminergic neurons. Understanding Neuronal Recycling Imagine two workers in a neuronal recycling plant. It’s their job to recycle mitochondria, the energy producers of the cell, that are too old or overworked. If the dysfunctional mitochondria remain in the cell, they can cause cellular dysfunction. The process of recycling or removing these old mitochondria is called mitophagy. The two workers in this recycling process are the genes Parkin and PINK1. In a normal situation, PINK1 activates Parkin to move the old mitochondria into the path to be recycled or disposed of. It has been well-established that people who carry mutations in both copies of either PINK1 or Parkin develop Parkinson’s disease because of ineffective mitophagy. A Tale of Two Sisters Two sisters had the misfortune of being born without the PINK1 gene, because their parents were each missing a copy of the critical gene. This put the sisters at high risk for Parkinson’s disease, but one sister was diagnosed at age 16, while the other was not diagnosed until she was 48. The reason for the disparity led to an important new discovery by Krainc and his group. The sister who was diagnosed at 16 also had partial loss of Parkin, which, by itself, should not cause Parkinson’s. “There must be a complete loss of Parkin to cause Parkinson’s disease. So, why did the sister with only a partial loss of Parkin get the disease more than 30 years earlier?” Krainc asked. As a result, the scientists realized that Parkin has another important job that had previously been unknown. The gene also functions in a different pathway in the synaptic terminal — unrelated to its recycling work— where it controls dopamine release. With this new understanding of what went wrong for the sister, Northwestern scientists saw a new opportunity to boost Parkin and the potential to prevent the degeneration of dopamine neurons. “We discovered a new mechanism to activate Parkin in patient neurons,” Krainc said. “Now, we need to develop drugs that stimulate this pathway, correct synaptic dysfunction and hopefully prevent neuronal degeneration in Parkinson’s.” Reference: “Parkinson’s disease linked parkin mutation disrupts recycling of synaptic vesicles in human dopaminergic neurons” by Pingping Song, Wesley Peng, Veronique Sauve, Rayan Fakih, Zhong Xie, Daniel Ysselstein, Talia Krainc, Yvette C. Wong, Niccolò E. Mencacci, Jeffrey N. Savas, D. James Surmeier, Kalle Gehring and Dimitri Krainc, 15 September 2023, Neuron. DOI: 10.1016/j.neuron.2023.08.018 The first author of the study is Pingping Song, research assistant professor in Krainc’s lab. Other authors are Wesley Peng, Zhong Xie, Daniel Ysselstein, Talia Krainc, Yvette Wong, Niccolò Mencacci, Jeffrey Savas, and D. James Surmeier from Northwestern and Kalle Gehring from McGill University. This work was supported by National Institutes of Health grants R01NS076054, R3710 NS096241, R35 NS122257 and NS121174, all from the National Institute of Neurological Disorders and Stroke.

The enzyme STARD7 (green) helps mitochondria (red) to transport Coenzyme Q to protect cells from cell death. Credit: MPI f. Biology of Aging/ S. Deshwal The Distribution of Coenzyme Q Within a Cell Is Regulated by Mitochondria Antioxidants are frequently touted as a panacea in the realm of nutrition and sold as dietary supplements. Nevertheless, our bodies naturally produce these free radical neutralizers, one of which is Coenzyme Q. Scientists from the Max Planck Institute for Biology of Aging in Cologne, Germany, have now uncovered how this substance, which is produced in our mitochondria, travels to the cell membrane and protects our cells from dying. Coenzyme Q is a crucial antioxidant for our bodies. A lack of Coenzyme Q can result in severe illnesses like Leigh syndrome, a hereditary condition that affects specific areas of the brain and can cause muscle weakness, among other symptoms. Additionally, a shortfall of Coenzyme Q is one of the earliest indications of aging and can occur as early as the early twenties. So, why can’t we simply consume this substance through our diet? “Coenzyme Q is a highly hydrophobic molecule that our bodies absorb very little from food,” explains Soni Deshwal, scientist at the Max Planck Institute for Biology of Aging and lead author of the study. But it is also a problem in our cells that coenzyme Q is not water soluble. The antioxidant is formed in mitochondria and must pass through the watery cell interior called cytoplasm to the surface of the cells in order to neutralize oxidized lipid species. “With our research, we have now been able to identify the proteins involved in coenzyme Q transport from the mitochondria to the cell surface,” explains Deshwal. The researchers found that an enzyme called STARD7 helps transport the coenzyme. This protein is not only localized in the mitochondria, but also inside the cytoplasm. Band-Aids for the Cell Surface “The mitochondria actively transport coenzyme Q to the cell surface to protect cells from cell death. It is as if the mitochondria deliver band-aids to the surface to protect the cell,” says Deshwal. “This again shows that mitochondria are not only important as an energy supplier for our cells, but also play crucial regulatory roles.” In the long term, the researchers hope that a precise understanding of this transport process will enable Coenzyme Q to be delivered into the cells of affected patients and thus provide a new therapeutic approach for diseases such as Leigh syndrome. Reference: “Mitochondria regulate intracellular coenzyme Q transport and ferroptotic resistance via STARD7” by Soni Deshwal, Mashun Onishi, Takashi Tatsuta, Tim Bartsch, Eileen Cors, Katharina Ried, Kathrin Lemke, Hendrik Nolte, Patrick Giavalisco and Thomas Langer, 19 January 2023, Nature Cell Biology. DOI: 10.1038/s41556-022-01071-y

Recent findings reveal that early mouse embryos replicate their DNA in a unique, uniform manner, which changes after the embryo grows beyond four cells. This early-stage replication is slower and more prone to errors, potentially impacting embryo development. New research shows that DNA replication in early mouse embryos doesn’t follow the expected patterns seen in older cells. A new discovery by researchers at the RIKEN Center for Biosystems Dynamics (BDR) in Japan upends decades of assumptions regarding DNA replication. Led by Ichiro Hiratani and colleagues, the experiments published August 28 in Nature show that DNA replication in early embryos is different from what past research has taught, and includes a period of instability that is prone to chromosomal copying errors. As failed pregnancies and developmental disorders are often related to chromosomal abnormalities the findings could impact the field of reproductive medicine, perhaps leading to improved methods of in vitro fertilization (IVF). Early Embryogenesis and DNA Replication During embryogenesis, the initially fertilized egg divides, as do each new set of daughter cells. By the third day after fertilization, an embryo has undergone three divisions and contains 16 cells. Each cell division is accompanied by DNA replication, ensuring that each daughter cell contains a copy of the whole genome. In their new study, the team of RIKEN BDR researchers set out to characterize the nature of the DNA replication process in early-stage embryos. They used their homemade single-cell genomics technique called scRepli-seq and applied it to developing mouse embryos. With this technology, the team was able to take snapshots of single embryonic cell DNA at different times during the DNA-replication periods. What they found contradicted what scientists have assumed about DNA replication in embryos. “We found multiple specialized types of DNA replication during early mouse embryogenesis, which no one has seen before,” says Hiratani. “In addition, we also found that at certain points, genomic DNA is temporarily unstable and chromosomal aberrations are elevated.” Discovery of Unique Replication Patterns in Early Embryos Textbooks tell us that DNA doesn’t replicate all at once. Instead, different regions of a chromosome are duplicated in a specific sequence. The team’s first discovery was that the replication-timing domains observed in mature cells do not exist until an embryo has 4 cells. This means that unlike any other cells in an eventual body, DNA is replicated uniformly, not sequentially, in 1- and 2-cell embryos. Each time a part of a chromosome unwinds for replication, regions of DNA unzip forming a structure that looks like a fork in the road. For replication to proceed, the fork must move down the strand of DNA, rezipping copied regions and unzipping the next section. The team’s second discovery was that fork speed is much slower in the 1, 2, and 4-cell stages than after the 8-cell stage of embryogenesis. The 4-cell embryo can now be seen as a transitional stage during which uniform DNA replication becomes sequential, while still showing slow fork movement characteristic of 1- and 2-cell embryos. In contrast, 8-cell embryos are much more similar to mature cells, showing sequential replication and fast fork movement. Implications of DNA Replication Errors Errors in DNA replication in the first few days after fertilization often result in chromosome irregularities, such as extra copies, missing copies, breaks in copies, or incomplete copies. Some of these copying mistakes lead to miscarriage, while others lead to developmental disorders like Down syndrome, also known as trisomy 21. The team’s third discovery was that the frequency of chromosomal copying errors was temporarily elevated in early-stage embryos, most commonly during the 4-cell stage. The researchers again used scRepli-seq, this time for detecting chromosome copy number abnormalities. They found that very few errors occurred during the transition between 1- and 2-cell stages or between 8- and 16-cell stages. On the other hand, 13% of cells showed chromosomal abnormalities during the transition between the 4- and 8-cell stages, likely due to copying errors during the 4-cell stage. Further testing suggested that the copying errors at this stage were related to the slow-moving forks. Future Research and Clinical Applications “Our findings lead to many new questions,” says Hiratani. “For example, are these series of phenomena evolutionarily conserved in other species, including human embryos? And what are the subsequent fates of cells with chromosomal aberrations?” In addition to guiding basic research in the future, this discovery could help fertilization clinics devise better strategies for minimizing the chromosomal abnormalities that are common in the first few days after fertilization. Reference: “Embryonic genome instability upon DNA replication timing program emergence” by Saori Takahashi, Hirohisa Kyogoku, Takuya Hayakawa, Hisashi Miura, Asami Oji, Yoshiko Kondo, Shin-ichiro Takebayashi, Tomoya S. Kitajima and Ichiro Hiratani, 28 August 2024, Nature. DOI: 10.1038/s41586-024-07841-y

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