Table 2. Some transcription factors in browning.

Transcription factor	Role in browning/thermogenesis	Interactions
UCP1	Key marker of browning and thermogenesis. Activates heat production in adipocytes.	Regulated by free fatty acids (activates) and purine nucleotides (inhibits). Transcription regulated by various factors (e.g., PRDM16, PPARγ) (Macher et al., 2018; Jash et al., 2019).
PPARγ	Regulates both fat and carbohydrate metabolism. Plays a role in adipogenesis and lipid storage. Can induce browning under certain conditions.	Interacts with LXR and RIP140 to downregulate UCP1. Agonists increase insulin sensitivity and browning but can also increase adiposity (Machado et al., 2022; Wang et al., 2008).
PGC-1α	Key factor for mitochondrial biogenesis. Stimulates thermogenesis in muscle and brown adipocytes.	Activated by β-adrenergic receptor stimulation. Regulates UCP1 and other thermogenic genes. Stimulated by exercise, cold, and pharmacological agents (Deng et al., 2019; Ishibashi & Seale, 2015).
CIDEA	Prevents downregulation of UCP1, thus promoting browning and thermogenesis.	Inhibits LXR to prevent UCP1 downregulation (Jash et al., 2019).
PRDM16	Activates thermogenic genes in WAT. Essential for the browning of subcutaneous WAT.	Stimulates PGC-1α expression and is necessary for maintaining beige adipocytes. Low PRDM16 expression can reverse browning (Harms et al., 2014; Ishibashi & Seale, 2015).

Note:

CIDEA, Cell Death-Inducing DNA Fragmentation Factor-Like Effector A; LXR, Liver X receptor; PGC-1α, Peroxisome Proliferator-Activated Receptor γ Co-Activator 1α; PPARγ, Peroxisome Proliferator-Activated Receptor γ; PRDM16, PR Domain Containing 16; RIP140, receptor-interacting protein 140; UCP1, Uncoupling Protein 1; WAT, white adipose tissue.