Fig 2: Immunohistochemistry of 12 selected genes expression in two lung adenocarcinoma cases. (A–L) Representative pictures of an IHC staining with paraffin-embedded tissue sections demonstrate the selected genes’ protein expression patterns (brown signal) in adjacent tissue (left panel) and matched malignant tumor tissue (right panel). The 12 selected genes were in order as follows: ADIPOR1, ARRB1, S100A12, CD1b, HAMP, HMOX1, KL, S100A7, S100A2, VEGFA, VIPR1, and TUBB3.

Fig 3: Role of AdipoRon in the expression of AdipoR1 and p-AMPK and ER stress in the kidneys of db/db mice. (a) Representative immunofluorescence images of AdipoR1 (A–C), GRP78 (D–F), and CHOP (G–I) in the renal tissues of three mouse groups. n = 8 per group. Bars = 100 µm. (b) Semiquantitative analysis of AdipoR1 and p-AMPK expression. (c) Semiquantitative analysis of nuclear CHOP positive cells (%). (d) Representative immunoblots of AdipoR1, p-AMPK, and T-AMPK. ß-Actin was used as a loading control. (e) Relative band intensity. (f) Representative immunoblots of GRP78, p-PERK, PERK, and CHOP. (g) Relative band intensity. n = 8 mice per group. The data are shown as the means ± SDs. *P < 0.05 versus db/m control mice; #P < 0.05 versus db/db mice. AdipoR1: adiponectin receptor 1; GRP78: glucose-regulated protein of 78 kDa; CHOP: C/EBP homologous protein; p-AMPK: phosphorylated 5'AMP-activated kinase; PERK: protein kinase-like endoplasmic reticulum kinase; p-PERK: phospho-PERK.

Fig 4: Proposed model for aerobic exercise’s alleviation of abnormal autophagy in brain cells of APP/PS1 mice by upregulating the AdipoR1 levels (created with BioRender.com). Available online: https://app.biorender.com/illustrations/6279e002dbc8411b3f12fe3f (accessed on 22 July 2022) Aerobic exercise upregulates AMPK and TFEB activity by upregulating the AdipoR1 levels in the brains of APP/PS1 mice, enhances lysosomal function, and improves abnormal autophagy, thereby alleviating AD-like lesions, Aß deposition, and cognitive dysfunction.

Fig 5: AdipoR1 is involved in IR-induced ferroptosis in HCC cells. (a) MHCC-97H cells were pretreated with different inhibitors of cell death 3-MA, ZVAD, Rapa, and Fer-1 and irradiated. The cell viability was detected by CCK-8 kit. (b–e) After treatment with 10 Gy for 48 h, lipid peroxidation was assessed by flow cytometry using C11-BODIPY in AdipoR1 knockdown MHCC-97H (b and c) and HepG2 (d and e) cells, respectively. (f and g) qRT-PCR showed the mRNA level of PTGS2 in HCC cells after radiation or AdipoR1 knockdown. Data is presented as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.