Table 1.

Summary of study results related to macrophages and Wnts in tissue injury and repair.

Organ/Tissues	Tissue-Resident Macrophages/Cells	Injuries/Diseases	Macrophages and Wnts	References
Lung	Alveolar macrophages	Pulmonary fibrosis	Activation of Wnt/β-catenin signaling in alveolar macrophages leading to disruption of repair and promotion of fibrosis in lung	[41,42,43]
		Mycobacterial infection	Wnt6 causing macrophage polarization with M2-like phenotypes	[44]
		Inflammatory injury	Exacerbation of inflammatory injury due to inhibition of anti-inflammatory interstitial macrophage, Influence of a pro-inflammatory Wnt5a ligand on M1/M2 macrophage polarization	[45,46]
		Chronic obstructive pulmonary disease	Increased contribution of macrophages on inflammatory response due to activation of Wnt5a/JNK1 pathway, Change in macrophage activity via activation of Wnt/β-catenin signaling	[47,48,49]
		Lung cancer	Transition to tumor-promoting M2-like tumor-associated macrophage due to Wnt/β-catenin-mediated transcriptional activation	[51]
Liver	Kupffer cells	Chronic liver disease (e.g., liver fibrosis)	The anti-fibrotic potential of Wnt derived from macrophages, Reduction in collagen accumulation and macrophage infiltration in inhibition of canonical Wnt pathway	[54,56]
		Pediatric nonalcoholic fatty liver disease (NAFLD)	Correlation of pro-inflammatory macrophage activation and hepatic progenitor cell response through Wnt3a pathway in NAFLD	[55]
		Partial hepatectomy	Wnt secretion from Kuffer cells for β-catenin activation for liver regeneration	[57]
		Mycobacterial infection	Control of mycobacterial infection in macrophage via FOXO1/Wnt5a signaling	[58]
		Hepatic inflammation	Promoted liver inflammation caused by modulation of Wnt signaling via LRP1 expression in macrophages	[59]
		Liver cancer	Stimulation of M2-like macrophage polarization through the canonical Wnt signaling of cancer cell-derived Wnt ligands, Promotion of tumor cell growth by Wnt/β-catenin signal induced by high-fat diet lipid accumulation and steatosis-induced macrophage infiltration	[60,61]
Intestine	Intestinal macrophages	Radiation injury	Macrophage-derived Wnts, an essential element for intestine regeneration	[64]
		Inflammatory bowel disease (IBD) (e.g., ulcerative colitis)	Activated Wnt signaling in epithelial cells caused by M2 macrophage through Wnt1, which impaired enterocyte differentiation, Promoting mucosal repair via the Wnt signaling pathway of STAT6-dependent macrophage	[65,66]
		Colorectal adenocarcinoma	Increased CD206-positive M2 macrophages and exaggerated Wnt signaling in colorectal cancer	[65,67]
Kidney	Renal macrophages	Kidney-ischemia-reperfusion injury	Stimulation of renal repair and regeneration of macrophage-derived Wnt7b	[72]
		Acute kidney injury	Wnt ligand generation and canonical Wnt signaling activity in macrophages after kidney injury	[73]
		Renal fibrosis	Stimulation of M2 macrophage polarization causing renal fibrosis due to increased Wnt signaling	[74,75,76]
Heart	Cardiac macrophages	Myocardial infarction (MI)	Macrophage as a source of non-canonical Wnt after MI Reduction in dramatic inflammation and improvement in the repair by M2 macrophage	[81,82]
Skin	Langerhans cells	Wound-induced hair neogenesis, Human hidradenitis suppurativa	Phagocytosis of macrophages on dermal Wnt inhibitor SFRP4	[86]
		Wound angiogenesis	Inhibition of angiogenesis and repair using Wnt-Calcineurin-Flt1 signaling in macrophages	[87]
		Hair growth	Increase in macrophage-derived Wnts in the hair growth cycle	[88,89]