New research unveils key molecular pathways in diabetic neuropathy and nephropathy

In a groundbreaking review published in Current Molecular Pharmacology, researchers from Teerthanker Mahaveer University have mapped the molecular mechanisms behind diabetic neuropathy and nephropathy, two severe complications of diabetes. The study, led by Dr. Phool Chandra, reveals how hyperglycemia triggers oxidative stress, inflammation, and metabolic dysregulation, leading to nerve and kidney damage.

"Understanding these pathways is crucial for developing targeted therapies," said Dr. Chandra. The team identified key players like protein kinase C (PKC), NADPH oxidase, and advanced glycation end-products (AGEs), which exacerbate nerve degeneration and renal fibrosis. For instance, PKC-β inhibitors like ruboxistaurin showed promise in reducing albuminuria in preclinical models.

The review also highlights the role of inflammatory cytokines like TNF-α and IL-6 in neuropathic pain and kidney injury. "Targeting these cytokines could halt disease progression," noted co-author Dr. Nikita Saraswat. Autophagy dysregulation and Wnt/β-catenin signaling were additionally implicated in nerve damage, offering new avenues for intervention.

Current treatments, such as anticonvulsants for neuropathy, provide symptomatic relief but fail to address root causes. The study advocates for multi-target therapies, including antioxidants and PKC inhibitors, to mitigate oxidative stress and inflammation. "Combining these approaches could revolutionize diabetic complication management," Dr. Chandra added.