Hdac4, histone deacetylase 4, is a specific class II histone deacetylation protein. It participates in epigenetic modifications, deacetylating heat shock proteins and various transcription factors. It is involved in numerous biological processes related to the central nervous system, bone, muscle, and metabolism [1,4].

In ischemic stroke, Hdac4 is dysregulated and impacts neuronal death, angiogenesis, and neurogenesis, playing a key role in the pathogenesis and post-stroke recovery [2]. In pancreatic cancer, m6A methylation affects Hdac4 stability, promoting glycolytic metabolism and migration. Also, Hdac4 mediates smoking-induced pancreatic cancer metastasis [3,5]. In anorexia nervosa, a missense mutation in Hdac4 was found in an affected family, and methylation differences were observed in AN patients [4]. In Th17 cell differentiation, Hdac4 and Hdac7 cooperate to regulate gene transcription [6]. Hdac4 also influences the DNA damage response, counteracting senescence by assembling with Hdac1/Hdac2 to control H2BK120 acetylation and homology-directed repair [7]. In preeclampsia, knockdown of Hdac4 triggers cell autophagy and apoptosis in placental trophoblast cells via miR-29b [8].

In summary, Hdac4 is crucial in multiple biological processes and disease conditions. Studies, including those using potential gene knockout mouse models (not explicitly detailed in provided refs but inferred from context), help reveal its functions in diseases like ischemic stroke, pancreatic cancer, anorexia nervosa, Th17-related inflammation, senescence, and preeclampsia, providing potential therapeutic targets.