hepato.site

Normal human liver: reticulin stain with zones labelled. Portal triad (Zone 1) to central vein (Zone 3). Hepatocyte plates outlined in reticulin fibres.

Boyd A, Cain O, Chauhan A, Webb GJ · CC BY 4.0

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Macrovesicular steatosis in NAFLD/MASLD. Trichrome stain: large lipid vacuoles (white) displace hepatocyte nuclei; pericellular fibrosis in blue-green; central vein centre-right.

Nephron · CC BY-SA 3.0

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Steatohepatitis (MASH). Trichrome stain at high magnification: ballooned hepatocytes, microvesicular and macrovesicular steatosis, lobular inflammation, chicken-wire pericellular fibrosis.

Nephron · CC BY-SA 3.0

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Ultrastructure of hepatocytes of animals of the control group. RER--rough endoplasmic reticulum, BC--bile canaliculi, GC--Golgi complex, CC--cell-cell contact, L--lipid droplet, Lys--lysosome, M--mitochondrion, N--nucleus. TEM, x5500.

Areshidze DA, Kozlova MA, Anurkina AV et al. Int J Mol Sci 2026 · CC BY 4.0

PMID 41898526 · fig. Fig. 4

Ultrastructure of hepatocytes of animals of the dark-deprivation group (constant artificial lighting, 3 months). G--glycogen, RER--granular endoplasmic reticulum, L--lipid droplet, M--mitochondria, Mph--macrophage, Ch--chromatin, N--nucleus, Nc--nucleolus. TEM, x5000.

Areshidze DA, Kozlova MA, Anurkina AV et al. Int J Mol Sci 2026 · CC BY 4.0

PMID 41898526 · fig. Fig. 5

Liver histology from rats. (A) Histological sections of liver tissue. Stain: hematoxylin and eosin. Scale bar: 20 μm. (B) Quantification of liver steatosis score. Values are presented as box plots with whiskers from minimum to maximum (n = 5/group). *p < 0.05 effect of diet; # p < 0.05 effect of Tucum-do-Cerrado.

Cavalcanti, Damazo, Arruda et al 2026, Molecular Nutrition and Food Research · CC BY 4.0

PMID 42377995 · fig. FIGURE 5

Optimization of ex vivo liver slice culture conditions. Viability was assessed by H&E staining after three days of culture under different conditions: (A) slice thickness comparison between 150 and 250 µm, n = 8 independent donors; (B) high oxygen partial pressure, 85% O₂ vs atmospheric, n = 11 independent donors; (C) air–liquid interface using porous inserts, n = 8 independent donors; and (D) matrix embedding assessed by cell efflux into the medium, n = 6 independent donors.

Feng, Esposito, Benjak et al 2026, Advanced Science · CC BY 4.0

PMID 42371767 · fig. FIGURE 2

Figure 7. Histopathological and ultrasound aspect of normal FT liver. (A): Normal histological appearance of the FT liver, demonstrating the UV, LSPV, PS, RAPV, RPPV. Classic hematoxylin-eosin staining, ×100

Nagy, R.D.; Ruican, D.; Zorilă, G.-L.; Istrate-Ofiţeru, A.-M.; Badiu, A.M.; Iliescu, D.G. · CC BY 4.0

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Figure 6. Histological appearance of the FT liver with normal PVS. (A): Histopathological aspect of FT fetal liver. It is observed how UV enters the hepatic structure (yellow arrow) and reaches its visceral surface near the intestinal loops

Nagy, R.D.; Ruican, D.; Zorilă, G.-L.; Istrate-Ofiţeru, A.-M.; Badiu, A.M.; Iliescu, D.G. · CC BY 4.0

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Brightfield imaging of hepatic cell seeding in MPS Pass / Fail. (A) 4-24 h after seeding of the MPS with hepatic cells they should show a cobblestone morphology with pronounced bright borders where cell-to-cell contacts occur to receive a passing score for cell attachment. (B) Example of a hepatic lot of primary human cells that failed to show strong adhesion even after a 24-hour attachment period

Varmazyad, Gavlock, Castiglione et al 2026, BMC Methods · CC BY 4.0

PMID 41669373

Body weight and hepatic lipid content. A ) In comparison with control animals, mice on CDD gain less weight whereas those on MCDD lose weight. B ) Hepatic liver triglyceride content was increased on both CDD and MCDD diets. C ) Liver weight was reduced in MCDD fed mice but not CDD. D ) Liver histology from control, CDD and MCDD mice. H+E = Hematoxylin and Eosin staining showing marked macrovesicular steatosis in both CDD and MCDD mice (white arrows). PSR = Picosirius Red stain staining for new collagen formation showing increased periportal and interstitial fibrosis in MCDD animals (black arrows). In MCDD liver stained with PSR, insert at higher magnification shows increased fibrosis more clearly. E ) Quantified fibrosis content (PSR positive staining as a percentage of entire image). n = 10 per group for all figures. * P < 0.05 ** P < 0.01 (one way ANOVA with Tukey post hoc test versus control animals). Error bars = +/- SEM.

Lyall, Cartier, Richards et al 2017, Wellcome Open Research · CC BY

PMID 29707653

Mouse liver portal triad: bile duct, hepatic artery, portal vein, and lymphatic vessels surrounded by hepatocytes. Staining method not stated. Mouse.

Bonnardel Johnny · CC BY-SA 4.0

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hepato/hepato-tem-organelles-control-1.webp

Transmission electron micrograph of rat hepatocyte ultrastructure (control group) showing mitochondria, rough endoplasmic reticulum, peroxisomes, and glycogen granules. Mohamed et al. 2026

Mohamed, Sabry, Elmistekawy et al 2026, Frontiers in Pharmacology · CC BY 4.0

PMID 42625669 · fig. FIGURE 11

hepato/hepato-sinusoid-disse-tem-1.jpg

TEM of the sinusoidal face of a Bactrian camel hepatocyte showing hepatocyte villi, mitochondria, granular ER, lipid droplet, fenestrated endothelial cell processes, and the perisinusoidal space of Disse. Musina et al. 2025

Musina, Lebedeva, Drozdova et al 2025, Animals (MDPI) · CC BY 4.0

PMID 41096516 · fig. Figure 4

hepato/hepato-tem-nucleus-ger-1.jpg

TEM of Bactrian camel hepatocyte interior showing nucleus with nucleolus, mitochondria, granular ER, lipid droplet, and free ribosomes. Musina et al. 2025

Musina, Lebedeva, Drozdova et al 2025, Animals (MDPI) · CC BY 4.0

PMID 41096516 · fig. Figure 7

hepato/hepato-tem-mitophagy-mouse-1.jpg

TEM of mouse hepatocytes showing autolysosomes (AL), mitochondria (M), endoplasmic reticulum (ER), lipid droplets (LD), and nucleus (N) in a mitophagy context (APAP injury model). Xu F et al. 2026

Xu, Albadry, Dirsch et al 2026, Clinical and Experimental Medicine · CC BY 4.0

PMID 42397441 · fig. Fig. 9

hepato/hepato-tem-mitochondria-cristae-1.jpg

TEM of primary hepatocyte mitochondrial ultrastructure under lipotoxic stress: intact cristae in controls versus swelling, disrupted cristae, and vacuolar degeneration under palmitic acid treatment (NAFLD model). Xue LJ et al. 2026

Xue, Yao, Fan et al 2026, Journal of Cell Communication and Signaling · CC BY 4.0

PMID 42368425 · fig. FIGURE 6

/images/cyto/hepa-bc-bsep-f3.jpg

F-Actin co-localizes with the canalicular marker BSEP in bile canaliculi. Immunofluorescence of human control liver tissue showing BSEP-positive bile canaliculi (apical belt between hepatocytes) with F-Actin co-staining. The canalicular network is visible as a polygonal belt between adjacent hepatocytes. Human liver. Scale bar indicated.

Mayer C 2023, EMBO reports · CC BY 4.0

PMID 37522754 · fig. Figure S6 (extended data)

/images/cyto/hepa-bc-zo1-f2.jpg

Hepatocytes of PSC patients accumulate apical bulkheads in bile canaliculi. Immunofluorescence showing ZO-1 (tight junction marker outlining bile canaliculi) and F-Actin co-staining. PSC patient hepatocytes show apical bulkheads compared to the normal canalicular network. NOTE: disease state (primary sclerosing cholangitis); the normal control panel shows the standard polygonal belt. Human liver.

Mayer C 2023, EMBO reports · CC BY 4.0

PMID 37522754 · fig. Figure 4

/images/cyto/hepa-bc-myo5b-f4.jpg

Myo5b at the apical membrane of healthy control human hepatocytes (control panel). Laser-scanning immunofluorescence micrographs showing regular bile canaliculus morphology in control hepatocytes, with myo5b at the apical plasma membrane and actin outlining the canalicular belt with its microvilli. Use control panel only; MYO5B-PFIC panel shows disease.

Hess MW 2021, Journal of clinical medicine · CC BY 4.0

PMID 33924896 · fig. Figure 5

/images/cyto/hepa-bc-mrp2-f5.jpg

Normal apical MRP2 localisation at the bile canaliculus in healthy control human hepatocytes. Immunofluorescence showing MRP2 concentrated at the apical (canalicular) face, with actin outlining the canalicular belt. MRP2 is the primary bile salt efflux pump. Use control panel only.

Hess MW 2021, Journal of clinical medicine · CC BY 4.0

PMID 33924896 · fig. Figure 7

/images/cyto/hepa-bc-tem-f6.jpg

Immuno-gold transmission electron micrograph of a human control bile canaliculus (panel g, ctrl.) showing normal ultrastructure: canalicular lumen with microvilli, tight junctions, and surrounding hepatocyte membranes. Rab11 immunogold labelling (normal distribution). Scale bar = 500 nm (panel g). Measured lumen width from scale bar: approximately 0.8–1.25 µm (consistent with Itoshima 1980, PMID 7414279: ~1.5 µm including microvilli). Use panel g (ctrl.) for normal anatomy; panel a (bx #1) shows MYO5B-PFIC disease with dilated canaliculus.

Hess MW 2021, Journal of clinical medicine · CC BY 4.0

PMID 33924896 · fig. Figure 9

Increased E-cadherin expression relative to N-cadherin induces hepatic polarity. (A) Representative iSIM images of polarized Can 10 cells and unpolarized parental Fao cells. Cells were cultured for 3 days, then fixed, and stained with DAPI and antibodies against MDR1 and ZO-1. Yellow arrowheads indicate nonpolarized cells lacking MDR1- and ZO-1-positive structures. (B) Immunoblot analysis of E- and N-cadherin expression in Fao and Can 10 cells. (C) Normalized intensity ratios of N-cadherin, E-cadherin, and p120-catenin relative to tubulin in Fao and Can 10 cells. Values represent means +/- SD from three independent experiments. Ratios in Fao cells were set to 1.0. (D) Analysis of cell polarization in Can 10 and Fao cells. Cells were cultured for 3 days, then fixed, and stained with phalloidin, DAPI, and antibodies against radixin and ZO-1. iSIM images were shown in horizontal (xy) and orthogonal (xz) views. Note that the Fao cells indicated by yellow arrowheads contain phalloidin-positive structures located within the cells. (E) Quantification of Can 10 and Fao cells with various types of polarity and BC structures. Values are means +/- SD from four independent experiments (>=401 cells counted per sample). (F) Analysis of TJ protein localization and assembly in Can 10 and Fao cells stained with DAPI and antibodies against Par-3 and ZO-1. Representative iSIM images are shown. (G) Analysis of AJ protein localization and assembly in relation to F-actin in Can 10 and Fao cells stained with phalloidin, DAPI, and antibodies against E-cadherin and N-cadherin. Representative iSIM images are shown.

Hayase, Yang, Zhou et al 2026, The Journal of Cell Biology · CC BY 4.0

PMID 42201352 · fig. Figure 2

BC formation and elongation benefits from low matrix rigidity. (A) Merged mid and bottom planes (z-projection) of hepatocyte cultures plated either on collagen-I gel, on collagen-functionalized PAA gels of ~0.5 kPa, or ~20 kPa or on collagen-coated glass and overlaid with collagen-I gel and cultured for 3 days; ZO1 outlines BC, which are also enriched in F-actin. beta-cat, beta-catenin. Note that rigidity-dependent stress fiber formation at the plating surface was accompanied by reduced BC length fraction. (B) Quantification of BC length fraction for each condition. BC length fractions were compared between glass-gel and 0.5-20 kPa cultures at day 1, 2 and 3 upon O/L. (C) Average cell area of 3 day O/L cultures on the indicated matrices; note that only significant differences are indicated; comparisons between all other datasets were not significant. Data shown are mean +/- s.d. n = 3 or 4 (B); n = 3 (C). *** P < 0.001; ** P < 0.01; * P < 0.05 (one-way ANOVA with multiple comparisons). Scale bars: 50 um.

Cohen, Lazaro-Dieguez, Musch et al 2025, Journal of Cell Science · CC BY 4.0

PMID 41347643 · fig. Fig. 2

Ultrastructural observations of autophagy-related structures in hepatocytes (A-C) and splenic macrophages (D-F) before and after starvation in T. rosa. (A,D) Cells with a normal structure before starvation; (B,E) after 30 days of starvation; (C,F) after 90 days of starvation. (a-f) Higher-magnification views of regions indicated by red squares in (A-F), respectively. Red arrows indicate autophagosome-like structures, and black arrows indicate autolysosome-like structures. Mit: mitochondrion, N: nucleus, RER: rough endoplasmic reticulum.

Wu, Ni, Xu et al 2026, Biology · CC BY 4.0

PMID 42589140 · fig. Figure 10

Characterization of the multi-polarization structure of expandable G-heporgs. A Immunostaining of Factin, ZO1, MRP2, and MDR1. Nuclei were stained with DAPI. Scale bar = 50 um. B, C 3D imaging of MDR1 and Factin staining. D Representative images of transmission electron micrograph (TEM). Scale bar = 2 um (left) and 500 nm (middle and right). Red arrows indicated microvilli, blue arrows indicated tight junction and yellow arrows indicated desmosomes. E Representative images of CDFDA staining. Scale bar = 100 um. F Representative images of Rho123 staining with or without Ver (Verapamil) treatment. Scale bar = 50 um.

Wu, Liu, Chen et al 2026, Cell Death & Disease · CC BY 4.0

PMID 41888105 · fig. Fig. 6

Validation of progenitor and hepatocyte marker expression in human liver organoids using confocal immunofluorescence analysis. (A) Representative confocal immunofluorescence images showing the expression of progenitor cell markers (LGR5 and EpCAM), and hepatocyte markers (A1AT, CYP3A4, HNF4A, and albumin) in human liver organoids (HLiOs) cultured under expansion or differentiation conditions. Nuclei were counterstained with DAPI (blue), while specific markers are shown in green or red. Scale bars: 50-100 um, as indicated. (B) Quantification of fluorescence intensity (RawIntDen) of progenitor and hepatocyte markers under expansion and differentiation conditions. Data are presented as fold changes relative to the expansion conditions. Data are shown as mean +/- SD from at least three independent experiments. *p < 0.05 was considered significant vs. expansion condition.

Cimino, Tinnirello, Orlando et al 2026, Frontiers in Cell and Developmental Biology · CC BY 4.0

PMID 42491280 · fig. FIGURE 2

Lutein modulates lipid accumulation and LC3 distribution in an in vitro model of steatosis. HepG2 cells were treated for 12 h with free fatty acids (FFAs) to induce steatosis and/or with lutein (10 uM). (A) Representative immunofluorescence images acquired by confocal microscopy with 3D reconstruction using Airyscan, showing LC3 (red), lipid droplets stained with BODIPY (green), and nuclei stained with Hoechst (blue). White arrows indicate LC3 colocalization with lipid droplets. (B) Quantification of BODIPY fluorescence intensity. (C) Quantification of LC3 fluorescence intensity. (D) Colocalization analysis between LC3 and BODIPY, expressed as Pearson's correlation coefficient, performed using ImageJ. Data are presented as mean +/- SEM of n = 3 independent experiments.

Saud, Cabrera, Valladares et al 2026, Antioxidants · CC BY 4.0

PMID 42650306 · fig. Figure 3

Lycopene restored mitochondrial function in the mice liver. (A) Transmission electron microscopy of mice liver. (B) ATP contents in liver tissue. (C) Mitochondrial membrane potential level. M: mitochondria; N: nucleus; yellow arrows: lipid droplets; red arrows: autolysosomes; red triangles: nascent mitophagosomes; red stars: mitophagosomes. NC: Normal control group; MC: Model control group; LL: Low-dose lycopene group, HL: High-dose lycopene group, FN: Fenofibrate group. Different lowercase letters indicate significant differences between groups (p < 0.05).

Xu, Wu, Ye et al 2026, Antioxidants · CC BY 4.0

PMID 42193269 · fig. Figure 5

Lycopene alleviate palmitic acid-induced hepatocyte lipotoxicity and mitochondrial dysfunction by improving mitophagy. (A) Oil Red O staining showing lipid accumulation in different groups, 50x. (B) Lipid droplets area of Oil Red O staining. (C) Mitochondria-ROS co-staining revealing oxidative stress levels. The red fluorescence from MitoSOX-Red indicates the production of mitochondrial ROS, with brighter red fluorescence indicating higher oxidative stress. (D) Mitochondrial superoxide production was assessed by MitoSOX Red staining (red fluorescence). Mitochondria were counterstained with Mito-Tracker (green fluorescence). Colocalization of MitoSOX Red and Mito-Tracker is shown in the merged images. Representative immunofluorescence images of cellular mitochondrial morphology; * p < 0.05, ** p < 0.001.

Xu, Wu, Ye et al 2026, Antioxidants · CC BY 4.0

PMID 42193269 · fig. Figure 7

Classification of TEM findings by intracellular organelles. Asterisk mitochondria; inside dotted line glycogen granules; arrow rER. As shown below, 0 was defined as normal, 1 as mildly abnormal, and 2 as highly abnormal. TEM findings of liver tissue are summarized in Table 2. a - c TEM of mitochondria. a Clear membrane/normal cristae = score 0, b Round shape/ruptured cristae = score 1, c Autophagosome formation/decrease in number = score 2, d - f TEM of glycogen granules. d Rich = score 0, e Decrease in number = score 1, f Complete loss = score 2, g - i TEM of rER. g Normal = score 0, h Expansion/degeneration = score 1, i Dissolution/spherical shape (loss) = score 2

Kido, Mizukoshi, Yanagi et al 2025, Journal of Gastroenterology · CC BY 4.0

PMID 40343540 · fig. Fig. 2

Loss of MIC13 disrupts the MIC10 subcomplex, crista junctions, and mitochondrial network morphology in iHeps. A Western blot analysis shows marked depletion of the MIC10-subcomplex (MIC10, MIC26, MIC27 and MIC13) in MIC13 mut iHeps, while the MIC60-subcomplex (MIC60, MIC19 and MIC25) remains largely unaffected, except for MIC25. B Representative TEM images of WT and MIC13 mut iHeps reveal abnormal cristae ultrastructure, including stacked or ring-like structure of the cristae. Scale bars: 500 nm. C Quantitative analysis of TEM images show that while the number of cristae per mitochondrial sections remains unchanged between WT and MIC13 mut iHeps, there is a significant reduction in number of CJs in MIC13 mut iHeps, indicating impaired cristae organization. Data is shown as separate violin plot with range, median and interquartile values indicated from approximately 135 sections from three independent (n = 3) experiments. Statistical analysis was performed using Student's t test. **** p <= 0.0001, ns = non-significant, p > 0.05. D Representative confocal images of WT and MIC13 mut iHeps immunostained for HSP60 (mitochondria, red) and counterstained with Hoechst (nuclei, blue) revealed extensive mitochondrial fragmentation in MIC13 mut iHeps. Yellow arrowhead indicate fragmented mitochondria and yellow lines traces tubular mitochondria. Scale bar: 10 um. E Quantification of mitochondrial network morphology, shown as a bar graph representing the percentage of cells displaying tubular, intermediate or fragmented mitochondria reveals a significant reduction in cells with tubular networks and a corresponding increase in cells with fragmented networks in MIC13 mut iHeps (around 50 cells per experiment, n = 3, mean +/- SEM). Statistical analysis was performed using Student's t test. * p <= 0.05, *** p <= 0.001, ns non-significant, p > 0.05. F Representative confocal microscopy images of WT and MIC13 mut iHeps immunostained with anti-DNA (mitochondrial nucleoids and nuclei, green) and anti-HSP60 (mitochondria, red), reveal no detectable alterations in nucleoid distribution within mitochondria in MIC13 mut iHeps. White arrow heads indicate mtDNA nucleoids within mitochondria. Scale bar: 10 um.

Becker, Eichmann, Vasiliev et al 2026, Cell Death & Disease · CC BY 4.0

PMID 42744797 · fig. Fig. 2

Loss of MIC13 disrupts the MIC10 subcomplex, crista junctions, and mitochondrial network morphology in iHeps. A Western blot analysis shows marked depletion of the MIC10-subcomplex (MIC10, MIC26, MIC27 and MIC13) in MIC13 mut iHeps, while the MIC60-subcomplex (MIC60, MIC19 and MIC25) remains largely unaffected, except for MIC25. B Representative TEM images of WT and MIC13 mut iHeps reveal abnormal cristae ultrastructure, including stacked or ring-like structure of the cristae. Scale bars: 500 nm. C Quantitative analysis of TEM images show that while the number of cristae per mitochondrial sections remains unchanged between WT and MIC13 mut iHeps, there is a significant reduction in number of CJs in MIC13 mut iHeps, indicating impaired cristae organization. Data is shown as separate violin plot with range, median and interquartile values indicated from approximately 135 sections from three independent (n = 3) experiments. D Representative confocal images of WT and MIC13 mut iHeps immunostained for HSP60 (mitochondria, red) and counterstained with Hoechst (nuclei, blue) revealed extensive mitochondrial fragmentation in MIC13 mut iHeps. Yellow arrowhead indicate fragmented mitochondria and yellow lines traces tubular mitochondria. Scale bar: 10 um. E Quantification of mitochondrial network morphology, shown as a bar graph representing the percentage of cells displaying tubular, intermediate or fragmented mitochondria.

Becker, Eichmann, Vasiliev et al 2026, Cell Death and Disease · CC BY 4.0

PMID 42744797 · fig. Fig. 2

Validation of progenitor and hepatocyte marker expression in human liver organoids using confocal immunofluorescence analysis. (A) Representative confocal immunofluorescence images showing the expression of progenitor cell markers (LGR5 and EpCAM), and hepatocyte markers (A1AT, CYP3A4, HNF4A, and albumin) in human liver organoids (HLiOs) cultured under expansion or differentiation conditions. Nuclei were counterstained with DAPI (blue), while specific markers are shown in green or red. Scale bars: 50-100 um, as indicated. (B) Quantification of fluorescence intensity (RawIntDen) of progenitor and hepatocyte markers under expansion and differentiation conditions. Data are presented as fold changes relative to the expansion conditions. Data are shown as mean +/- SD from at least three independent experiments. *p < 0.05 was considered significant vs. expansion condition.

Cimino, Tinnirello, Orlando et al 2026, Frontiers in Cell and Developmental Biology · CC BY 4.0

PMID 42491280 · fig. FIGURE 2

HFD diet induces liver injury and inhibits hepatic Pemt expression in large yellow croaker. (A) HE staining of liver sections in the Con and HFD groups (n = 4). Scale bars, 50 um. (B) Serum alanine aminotransferase (ALT) and (C) aspartate aminotransferase (AST) activities in the Con and HFD groups (n = 6). (D) The protein expression of apoptosis-related protein (Parp1, Cleaved-Parp1, Cleaved-Caspase3, Cleaved-Caspase9, Bax, and Bcl2) (n = 3) and (E) Nlrp3 inflammasome activation-related protein (Nlrp3, Cleaved-Caspase1, and mature Il1beta) in the liver of fish fed Con and HFD diets (n = 3). (F) Mitochondrial structure in the liver identified by TEM in fish fed Con and HFD diets. Red scale bars, 2 um, black scale bars, 1 um. M, mitochondria, LD, lipid droplet, N, nucleus. The results are presented as the mean +/- SEM. * p < 0.05, ** p < 0.01, and *** p < 0.001.

Bu, Cao, Yao et al 2026, Advanced Science · CC BY 4.0

PMID 42389879 · fig. FIGURE 1

Adhesion and 3D growth of primary hepatocytes on the surface of PVA NM in monoculture and coculture with NIH3T3 cells. (A) Primary hepatocytes were cultured on PVA NM in monoculture or coculture with NIH3T3 cells in a layer-by-layer culture system, and the cultures were observed using DIC microscopy. (B) Staining of live/dead cells with fluorescence. Green and red colors are observed in live and dead cells, respectively. (C) SEM images of monocultured and cocultured hepatocytes. The images represent three or four independent experiments and different magnifications.

Tran, Han, Tran et al 2026, International Journal of Molecular Sciences · CC BY 4.0

PMID 41828586 · fig. Figure 2

Rab1A deficiency alleviates western diet-induced hepatic steatosis in adult mice. (A) Experimental scheme for establishing WD-induced models with wild-type control (WT) and Rab1A knockout (KO) mice (n = 8). (B) ITT of mice after 16 weeks on the diet. Results are presented as mean +/- SEM (n = 8), *** p < 0.001, analyzed by two-way ANOVA. (C) Representative images of livers in WT and Rab1A KO mice on the diet in situ. White speckles indicate lipid accumulation. Scale bar, 1 mm. (D) Representative H&E staining of liver sections in WT and Rab1A KO mice on the diet. White holes indicate hepatic steatosis. Scale bar, 50 um. (E) Triglyceride levels in serum from 4 groups of mice were quantified using respective kits. Results are presented as mean +/- SEM (n = 8). *** p < 0.001, unpaired Student t-test for two groups. (F) AST from serum of 4 groups of mice was quantified using the respective kits. Results are presented as mean +/- SEM (n = 8). **** p < 0.0001, unpaired Student t-test for two groups. (G) Quantification of ALT in liver supernatants from WT and Rab1A KO mice on diet. Results are presented as mean +/- SEM (n = 8). * p < 0.05, ** p < 0.01, unpaired Student t-test. (H) Experimental design of WD-induced model in Rab1A liver-specific knockdown and control mice (n = 8). (I) Validation of Rab1A knockdown in liver upon AAV-shRab1A delivery by immunoblot. (J,K) GTT and ITT performed with Scramble and Rab1A knockdown mice (16 weeks on diet). Results are presented as mean +/- SEM (n = 7). ** p < 0.01, **** p < 0.0001, analyzed by two-way ANOVA. (L) Representative images of livers and ORO staining of liver sections with Scramble and Rab1A knockdown mice. Scale bar, 100 um. (M) Quantification of triglyceride levels in liver supernatants from Scramble and Rab1A knockdown mice on a diet. Results are presented as mean +/- SEM (n = 6). * p < 0.05, unpaired Student t-test. (N) Quantification of ALT in liver supernatants from Scramble and Rab1A knockdown mice on diet. Results are presented as mean +/- SEM (Scramble = 7, shRab1A = 5). **** p < 0.0001, unpaired Student t-test.

Zhang, Li, Zhang et al 2026, Advanced Science · CC BY 4.0

PMID 42801566 · fig. FIGURE 2

hTCL phenotype in proliferating primary hepatocyte cultures analyzed by LCI and SEM. The cultures were incubated in serum-free MEM supplemented with EGF (40 ng/mL) and insulin (0.9 ug/mL). (a) Phase contrast image of an hTCL locating to a hepatocyte where the soma (S) as well as the telopodium (Tp, white arrows; diameter of about 500 nm) with dilations (D; podomes) can be resolved. It is not clear whether the dark zone at the soma-Tp connection (S, black arrow) represents the nucleus (23 h 30 min after culture). (b,c) SEM inspection of hTCLs after 24 h of incubation; (b) two hTCLs locating to a hepatocyte membrane can be seen, one hTCL showing a very long Tp (white arrows) with several dilations (D). (c) Array of telopodia (white arrows) extending at a hepatocyte border (Hep; green arrows) to the collagen coat (Coll) also showing several dilations (D), Tp end-contacts to the cell surface (C), and distinct Tp-to-Tp contacts (insert). Annotated are two telopodia with diameters of 150 nm (a) and 286 nm (b) and a Tp-bundle of 430 nm diameter (c).

Bresgen, Kerschbaum, Kalyuzhny et al 2026, Cells · CC BY 4.0

PMID 42645210 · fig. Figure 3

Knockdown of Tph1 activates Parkin-mediated mitophagy and alleviates hepatic injury in MASLD mice. (A) TEM images showing mitochondrial ultrastructure in liver tissue. Scale bar = 5 um (B, C) Western blotting analysis and quantification of LC3 and p62 expression in total liver lysates ( n = 3 per group). (D, E) Western blotting analysis and quantification of LC3, Parkin, and p62 protein levels in mitochondrial fractions ( n = 3 per group). Data are presented as mean +/- SD. * P < 0.05; ** P < 0.01; *** P < 0.001. TEM, transmission electron microscopy; MASLD, metabolic dysfunction-associated steatotic liver disease; AAV, adeno-associated virus; NC, negative control.

Jia, Ye, Wang et al 2026, Pediatric Investigation · CC BY 4.0

PMID 42682592 · fig. FIGURE 4

Knockdown of Tph1 activates Parkin-mediated mitophagy and alleviates hepatic injury in MASLD mice. (A) TEM images showing mitochondrial ultrastructure in liver tissue. Scale bar = 5 um (B, C) Western blotting analysis and quantification of LC3 and p62 expression in total liver lysates (n = 3 per group). (D, E) Western blotting analysis and quantification of LC3, Parkin, and p62 protein levels in mitochondrial fractions (n = 3 per group). Data are presented as mean +/- SD.

Jia, Ye, Wang et al 2026, Pediatric Investigation · CC BY 4.0

PMID 42682592 · fig. FIGURE 4

Representative transmission electron microscopy (TEM) images of brown trout primary hepatocyte spheroids cultured for 8, 12, 18 and 25 days, at 18 degrees C and 21 degrees C (n = 3 spheroids/day/fish). DB: dense bodies, GA: Golgi apparatus, LD: lipid droplet, Mi: mitochondria, Nu: nucleus, Nc: nucleolus, RER: rough endoplasmic reticulum

Alves, Malhao, Lopes et al 2026, Cell and Tissue Research · CC BY 4.0

PMID 42443491 · fig. Fig. 7

TRPM2 gene knockout reduced lysosomal abundance in PA-treated primary hepatocytes. The primary cultured hepatocytes from TRPM2+/+ and TRPM2-/- were treated with PA (250 um for 24 h) to induce lipid accumulation or with BSA as a control. (A) The cells were co-stained with lysosome marker LysoTracker and neutral lipid dye BODIPY493/503 or (B) with lysosome marker LAMP1 and BODIPY493/503. Scale bar: 20 um as indicated. Representative of N = 10 slides from the cells prepared from 5 mice.

Ying, Zhuo, Zhou et al 2026, Cells · CC BY 4.0

PMID 42587771 · fig. Figure 3

H&E staining of normal liver tissue from four species (mouse, rat, pig, and human) showing lobular architecture. Central veins and portal tracts demarcate the lobular boundaries; hepatocytes are arranged in cords between sinusoids.

Albadry M 2024, Frontiers in pharmacology · CC BY 4.0

PMID 38818378

IHC showing zonation of GS, CYP1A2, CYP2D6, CYP2E1, and CYP3A4 in liver lobules from four species including human. Each marker shows characteristic pericentral or periportal distribution along the portal-central axis.

Albadry M 2024, Frontiers in pharmacology · CC BY 4.0

PMID 38818378

Overview of H&E and zonal expression in normal liver lobules from four species including human. GS-positive pericentral (zone 3) and CYP-positive periportal (zone 1) regions illustrate the functional gradient across the lobule.

Albadry M 2024, Frontiers in pharmacology · CC BY 4.0

PMID 38818378

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