Sarcoidosis, a granulomatous disease characterized by macrophage and T-cell activation, is found to be associated with increased HIF-1α transcriptional activity, and modulation of HIF-1α regulates inflammatory immune responses.

Hemodynamic forces regulate endothelial cell metabolism, which in turn regulates endothelial inflammation.

The long-distance flight of locusts is greatly facilitated by a muscle-abundantly expressed Hif-1α splice variant, which remains active in normoxia and scavenges flight-induced reactive oxygen species by upregulating the expression of DJ-1 (PARK 7).

The TIPE/PKM2/HIF-1α signaling pathway plays a crucial role in enhancing cancer stem cell properties by facilitating glycolysis, thereby presenting a promising therapeutic target for melanoma intervention.

Transcriptomic and bionergetic analysis shows the importance of HIF-1α activation in enabling tissue-resident alveolar macrophages to perform glycolytic metabolism, which prevents their death and attenuates influenza A virus-induced acute lung injury.

Hypoxia does not increase glycolysis in proliferating primary cells and antagonizes the increase in glycolysis caused by activation of hypoxia-inducible factor in normoxia, in part, through activation of MYC signaling pathways.

Live-cell single particle tracking reveals the intrinsically disordered regions of transcription factors playing an unanticipated role in the nuclear search and chromatin binding process leading to functional target site selectivity and gene activation.

A gene normally involved in responding to hypoxia helps to protect insect muscles during migratory flight in a non-oxygen dependent manner.

Macrophage Bmal1 controls the timing of the glycolytic to oxidative metabolism transition that dictates the extent of Hif-1a activation and the associated inflammatory response.

SIRT1 and SIRT3-mediated immunometabolic shift governs intracellular Salmonella proliferation both in vitro and in vivo and dissemination in mice, thereby influencing the infection outcomes.