Table 1.

Summary of key m⁶A regulators and their roles in wound healing and post-wound events

Type	Regulator	Biological process	Target	Sample	Biological function	References
m6A writers	METTL3	Diabetic wound	lncCCKAR-5	hUCMSCs, mice	METTL3-mediated m6A modification of lncCCKAR-5 enhances the formation of the lncCCKAR5/LMNA/MKRN2 complex and LMNA degradation in hUCMSCs, thereby inhibiting diabetic wound repair	100
		Keloid	Smad3	HTFs, New Zealand white rabbits	METTL3 promotes TGF-β/Smad signalling by upregulating Smad3, thus enhancing the viability, proliferation, and ECM deposition of HTFs	124
		Hair follicle	Wnt, Shh	Mouse skin epidermal progenitors, C57BL/6 mice	METTL3 ablation in epidermal progenitor cells leads to defects in Wnt and Shh signaling pathways, and reduced HF formation	134
		Hair follicle	SETD1A, SETD1B, KMT2B, KMT2D	C57BL/6 mice	METTL3-eKO newborn mice have abnormal epidermal development and deformed hair follicles.	135
		Keloid	Wnt3a, β-catenin, S100A4	HSFs, Human keloid tissue	Elevated METTL3 and WTAP upregulate the Wnt/β-catenin/S100A4 pathway in human keloid tissue	123
	ZC3H13	Keloid	HIPK2	HKFs, Human keloid tissue	Elevated ZC3H13 mediates the m6A modification and stabilisation of HIPK2, thereby promoting HKFs proliferation and accelerating keloid formation	125
	METTL14	Wound	PVT1	Mice	METTL14 modifies lncRNA PVT1 to stabilize MYC, thereby increasing the number of p63-positive basal cells and promoting wound healing	89
m6A readers	IGF2BP1	Diabetic wound	HMGB1	HUVECs	Increased expression of IGF2BP1 stabilises and increases the expression of HMGB1 mRNA, thereby promoting apoptosis in high glucose-induced HUVECs	147
	IGF2BP2	Wound	HPSE	HaCaT	IGF2BP2 enhances the stability of HPSE, promotes the proliferation and migration of HaCaT cells, and accelerates wound healing	91
		Wound	let-7b	HaCaT, Mice	The overexpression of let-7b inhibits the expression of IGF2BP2 in HaCaT cells, resulting in delayed epithelialisation and skin wound healing	92
	IGF2BP3	Wound	circCDK13	HDFs, HEKs	IGF2BP3 enhances circCDK13 to promote CD44 and c-MYC expression, which enhances the proliferation and migration of HDFs and HEKs and promotes wound healing	105
	YTHDC1	Diabetic wound	SQSTM1	HaCaT, Mice	Downregulation of YTHDC1 in HaCaT cells and mice accelerated SQSTM1 mRNA degradation, leading to delayed diabetic wound healing process	104
m6A erasers	ALKBH5	Hypertrophic scars	COL1A1, COL3A1, ELN	HDFs, Human HTS tissue	Defects in ALKBH5 lead to elevated m6A levels of COL3A1, COL1A1, and ELN, leading to pathological deposition and remodeling of the extracellular matrix	127
	ALKBH5 FTO	Wound	PELI2	HaCaT, Mice	ALKBH5 and YTHDF2 promote PELI2 expression, which promotes keratinocyte migration, epithelialization, and skin wound healing.	97
	FTO	Burn injury	TFPI-2	HaCaT, Rats	Overexpression of FTO inhibits TFPI-2 expression, which promotes the proliferation of thermally stimulated HaCaT cells and accelerates wound healing in burned rats	116
		Keloid	COL1A1, α-SMA	HDFs, Human keloid tissue	Overexpression of FTO in HDFs enhances the expression of COL1A1 and α-SMA, thereby promoting keloid formation	126
		Sweat gland	Nanog	MSCs	Inhibition of FTO expression by TNF-α leads to down-regulation of Nanog expression as well as a reduced potential for MSCs to differentiate into sweat glands.	138