Publications by authors named "Indira Martinez-Jimenez"

Cellular memory is a controversial concept representing the ability of cells to "write and memorize" stressful experiences via epigenetic operators. The progressive course of chronic, non-communicable diseases such as type 2 diabetes mellitus, cancer, and arteriosclerosis, is likely driven through an abnormal epigenetic reprogramming, fostering the hypothesis of a cellular pathologic memory. Accordingly, cultured diabetic and cancer patient-derived cells recall behavioral traits as when in the donor's organism irrespective to culture time and conditions.

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  • Diabetic foot ulcers (DFU) have high inflammation levels due to persistent high blood sugar and local infections, making healing difficult; epidermal growth factor (EGF) treatment has shown promise in promoting healing and reducing amputation risk.
  • The study focuses on the effect of EGF on fibroblasts taken from DFU, particularly how it counters inflammation induced by lipopolysaccharides (LPS) in a simulated hyperglycaemic environment.
  • Results indicate that EGF can reduce the inflammatory response in fibroblasts challenged by LPS, suggesting it may be beneficial for DFU treatment in real-life clinical scenarios.
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  • Lower-extremity arterial disease is a growing health issue that can result in amputations and increased mortality, but the underlying causes of vascular wall changes are not well understood.* -
  • Researchers hypothesized that a "vascular tissue memory" might be passed from humans to healthy animals through signaling molecules, leading to similar vascular issues like wall thickening in the recipient animals.* -
  • In experiments, injecting arteriosclerotic tissue into rats caused significant changes in their vascular structure within days, suggesting these changes are driven by factors from the human tissue, opening up new avenues for studying atherosclerosis.*
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Background: Diabetic foot ulcers are a common diabetic complication leading to alarming figures of amputation, disability, and early mortality. The diabetic glucooxidative environment impairs the healing response, promoting the onset of a 'wound chronicity phenotype'. In 50% of ulcers, these non-healing wounds act as an open door for developing infections, a process facilitated by diabetic patients' dysimmunity.

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  • Diabetes is rapidly increasing, leading to serious complications like lower limb ulcers and amputations due to impaired skin cell healing and resilience.
  • The condition creates a "senescent cells society," where aging and dysfunctional cells hinder the healing process, driven by factors like hyperglycemia and oxidative stress.
  • Effective treatment may involve targeting these senescent cells and their harmful secretions to improve healing outcomes for diabetic ulcers and prevent chronic wound development.
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