Lactate-Lactylation Axis as an Emerging Metabolic-Epigenetic Pathway in Diabetic Microvascular Complications - PubMed
4 hours ago
- #Epigenetics
- #Diabetic Complications
- #Lactylation
- Lactate is now recognized as a key signaling molecule and epigenetic regulator through lactylation.
- Diabetic microvascular complications (DR, DKD, DPN) involve excessive lactate production due to hyperglycemia-induced glycolysis.
- Lactate-lactylation axis contributes to mitochondrial dysfunction, chronic inflammation, and epigenetic alterations resembling premature aging.
- Lactylation reshapes gene transcription in retinal, renal, and peripheral nerve cells, influencing cellular dysfunction.
- In DR and DKD, lactylation affects microvascular cell types; in DPN, it may impact Schwann cells and axonal integrity.
- Lactate-driven epigenetic remodeling reinforces metabolic memory and tissue-specific aging despite glycemic control.
- Therapeutic potential exists in modulating lactylation pathways, with lactate as a possible biomarker.
- The lactate-lactylation axis links hyperglycemia to premature aging in diabetic microvasculature.