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cardiomyocyte

Real pictures of the cardiomyocyte delivered by gather.site, each with its paper.

15 pictures and 11 papers.

Gallery

(A-C) Representative immunostaining of sarcomeric markers, including alpha-actinin (green), cTnT (green), and myosin (green) in hiPSC-CMs. Cells cultured in FAM exhibit well-defined, aligned sarcomeric striations indicative of structural maturation, in contrast to the less organized morphology in GLM. Scale bar = 20 µm. (human (hiPSC-derived cardiomyocytes); Fig. 2, panels A-C (IF alpha-actinin, cTnT, myosin; FAM vs GLM hiPSC-CMs).)

Gaballah, Penttinen, Prajapati et al 2026, Cellular and Molecular Life Sciences · CC BY 4.0

Vitrified healthy control (WT1) iPSC-CM attached to the electron microscopy grid. Scale bar, 20 µm. (human (iPSC-derived cardiomyocyte); Fig. 3, panel a (healthy control WT1 iPSC-CM on cryo-EM grid; rows 6-390 of figure).)

Ignatyeva, Cheruiyot, Saleem et al 2026, Signal Transduction and Targeted Therapy · CC BY 4.0

Histological study of stained slides: Ischemic myocardium in rats. (A) Light microscopy with hematoxylin and eosin (H&E) staining, x200; (B) the same section, polarized light, intense anisotropic areas are visible in some cardiomyocytes, x200; (C) Mallory's trichrome staining, x200; (D) Lie staining (HBFP), some areas of early ischemia are visible, x200; (E) Weigert's iron hematoxylin staining, the striation of cardiac muscle tissue is visible, x800; (F-H) groups with cardiac arrest, sham intervention, and respiratory arrest, respectively. Ob. x40. Red arrows mark the Ki67+ cells. Scalebar 40 um; (I) the number of Ki67+ cells. (rat (ischemic myocardium, cardiac arrest, sham, and respiratory arrest groups); Figure 3.)

Piavchenko, Venediktov, Shamitko et al 2026, Journal of Biophotonics · CC BY 4.0

Detection of CAV3-CMs structure. (A) Immunofluorescence staining of cTnT and alpha-actin, red for cTnT, yellow for alpha-actin, blue for cell nucleus. (B) ImageJ software was used to measure sarcomere length in micrographs of differentiated cardiomyocytes. The yellow straight lines indicate the regions subjected to measurement. The bar graphs represent the statistical analysis of the sarcomere length measurements. (C) ImageJ software was employed to measure cell perimeter and cell area in micrographs of differentiated cardiomyocytes. The yellow lines trace the cell perimeter, and the areas enclosed by the yellow lines denote the cell areas. The bar graphs depict the statistical results of the sarcomere length measurements. (Figure 3.)

Wang, Zhu, Li et al 2026, Human Mutation · CC BY 4.0

Fatty acid substrates enhance the morphological and structural maturation, and upregulate gene and protein expression in hiPSC-CMs. (A-C) Representative immunostaining of sarcomeric markers, including alpha-actinin (green), cTnT (green), and myosin (green) in hiPSC-CMs. Cells cultured in FAM exhibit well-defined, aligned sarcomeric striations indicative of structural maturation, in contrast to the less organized morphology in GLM. Scale bar = 20 um. (D) Representative transmission electron microscopy images of GLM- and FAM-cultured hiPSC-CMs reveal improved alignment of myofilaments (MF) and Z-lines (Z), with more organized banding and sarcomeric structure in the FAM group. Key features are mitochondria (M), myofilaments (MF), Z-lines (Z), and nucleus (N). (E) Quantitative assessment of cell structural parameters. FAM-cultured hiPSC-CMs show significantly increased cell perimeter, cell area, and sarcomere length, along with a decreased circularity index, compared to GLM-cultured CMs (n = 40 cells from 3 independent experiments). (F) Quantitative real-time PCR analysis of structural gene expression. FAM-cultured CMs exhibit significantly elevated expression of TNNT2, TNNI3, MYH7, and MYBPC3. (H) Expression of fetally enriched genes MYH6, NPPB, and ACTA1 was significantly decreased in FAM-cultured CMs, indicating a more mature gene expression profile. *Data are presented as mean +/- SEM. (Fig. 2.)

Gaballah, Penttinen, Prajapati et al 2026, Cellular and Molecular Life Sciences · CC BY 4.0

Sarcomeric organization and tension in shape-patterned CMs. (a) Fluorescent images (clover) and FRET index of circular and rectangular patterned hiPSC-CMs in relaxation and contraction state. (b) Violin plots of sarcomere spacing, (c) distribution plot of FRET index, (d) violin plots of median FRET index/cell, (e) IQR, and (f) order parameter (arbitrary units) in circular (blue) and rectangular (orange) shaped hiPSC-CMs in relaxation and contracted state. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, by Kruskal-Wallis test; 32 < n < 78 cells per condition. (FIG. 2..)

Dutta, Toth, Sundaram et al 2026, APL Bioengineering · CC BY 4.0

Detection of CAV3-CMs structure. (A) Immunofluorescence staining of cTnT and alpha-actin, red for cTnT, yellow for alpha-actin, blue for cell nucleus. (B) ImageJ software was used to measure sarcomere length in micrographs of differentiated cardiomyocytes. The yellow straight lines indicate the regions subjected to measurement. The bar graphs represent the statistical analysis of the sarcomere length measurements. (C) ImageJ software was employed to measure cell perimeter and cell area in micrographs of differentiated cardiomyocytes. The yellow lines trace the cell perimeter, and the areas enclosed by the yellow lines denote the cell areas. The bar graphs depict the statistical results of the sarcomere length measurements. (Figure 3.)

Wang, Zhu, Li et al 2026, Human Mutation · CC BY 4.0

Fatty acid substrates enhance the morphological and structural maturation, and upregulate gene and protein expression in hiPSC-CMs. (A-C) Representative immunostaining of sarcomeric markers, including alpha-actinin (green), cTnT (green), and myosin (green) in hiPSC-CMs. Cells cultured in FAM exhibit well-defined, aligned sarcomeric striations indicative of structural maturation, in contrast to the less organized morphology in GLM. Scale bar = 20 um. (D) Representative transmission electron microscopy images of GLM- and FAM-cultured hiPSC-CMs reveal improved alignment of myofilaments (MF) and Z-lines (Z), with more organized banding and sarcomeric structure in the FAM group. Key features are mitochondria (M), myofilaments (MF), Z-lines (Z), and nucleus (N). (E) Quantitative assessment of cell structural parameters. FAM-cultured hiPSC-CMs show significantly increased cell perimeter, cell area, and sarcomere length, along with a decreased circularity index, compared to GLM-cultured CMs (n = 40 cells from 3 independent experiments). (F) Quantitative real-time PCR analysis of structural gene expression. FAM-cultured CMs exhibit significantly elevated expression of TNNT2, TNNI3, MYH7, and MYBPC3. (G) Western blot analysis of beta-MHC protein expression shows increased levels in FAM-cultured CMs. beta-actin was used as the loading control (n = 3 independent batches). *Data are presented as mean +/- SEM. Statistical analysis was performed using unpaired two-tailed Student's t-test. p < 0.05 indicates statistical significance. (Fig. 2.)

Gaballah, Penttinen, Prajapati et al 2026, Cellular and Molecular Life Sciences · CC BY 4.0

Fatty acid substrates enhance the morphological and structural maturation, and upregulate gene and protein expression in hiPSC-CMs. (A-C) Representative immunostaining of sarcomeric markers, including alpha-actinin (green), cTnT (green), and myosin (green) in hiPSC-CMs. Cells cultured in FAM exhibit well-defined, aligned sarcomeric striations indicative of structural maturation, in contrast to the less organized morphology in GLM. Scale bar = 20 um. (D) Representative transmission electron microscopy images of GLM- and FAM-cultured hiPSC-CMs reveal improved alignment of myofilaments (MF) and Z-lines (Z), with more organized banding and sarcomeric structure in the FAM group. Key features are mitochondria (M), myofilaments (MF), Z-lines (Z), and nucleus (N). (E) Quantitative assessment of cell structural parameters. FAM-cultured hiPSC-CMs show significantly increased cell perimeter, cell area, and sarcomere length, along with a decreased circularity index, compared to GLM-cultured CMs (n = 40 cells from 3 independent experiments). (human (hiPSC-derived cardiomyocytes from human induced pluripotent stem cells); Fig. 2.)

Gaballah, Penttinen, Prajapati et al 2026, Cellular and Molecular Life Sciences: CMLS · CC BY 4.0

Structural phenotyping of engineered laminar cardiac tissues. (a) Schematic of anisotropic laminar tissue formation using gelatin molds (ridge width 25 um, groove width 4 um, and groove depth 5 um) (i) and quantification of alignment by OOP (ii). (b) Representative bright-field and immunofluorescence images of NRVM tissues at day 7 stained for alpha-actinin (red), F-actin (white), and nuclei (blue). (c)-(g) Quantification of F-actin OOP, sarcomere OOP, sarcomere length, nuclear eccentricity, and orientation. (h) Representative images of micromolded hiPSC-CM tissues from 2D-Mono and 3D-EB cultures at days 7 and 14. (i)-(m) Comparative analysis of myofibrillar and nuclear organization in 2D-Mono and 3D-EB tissues on days 7 and 14. Scale bar: 50 um in (b) and (h). Values are presented as mean +/- SEM. (FIG. 2..)

Jang, Shani, Clouvel-Gervaiseau et al 2026, APL Bioengineering · CC BY 4.0

Sarcomere tracking in genetically engineered Z-line labeled induced pluripotent stem cell (iPSC)-derived cardiomyocytes (CMs) on micropatterned soft gels. (A) Sketch of a human CM adhering to a micropatterned gel (top) and sarcomere structure in relaxed and contracted state (bottom). (B) ACTN2-Citrine CMs (culture day 20) on a polyacrylamide gel substrate (Young's modulus: 15 kPa), patterned with rectangular stripes of Synthemax (70 x 10 um). More than 50% of the stripes were typically occupied by single CMs. Inset: zoomed-in view. (C) Tracking of sarcomere motion: (Top) Blend of high-speed confocal movie of a CM adherent to a 15-kPa substrate (left) and deep-learning (3D U-Net)-based segmentation of sarcomere Z-bands (right) with line of interest (LOI, yellow). (Bottom) Intensity extracted along LOI. Inset shows representative section of the Z-band intensity profile. (D, E) Confocal images of representative ACTN2-Citrine-labeled CMs with corresponding Z-band segmentation and LOIs (red lines). (G-I) Z-band trajectories tracked along the LOI. (J-O) Overlay plots of single-sarcomere length change dSL(t) for all tracked sarcomeres in the marked LOIs (first 5 s in J-L, zoomed in M-O). Colored lines are individual sarcomere length changes; black lines display average length changes. Contraction intervals are marked by a blue background. Sarcomere popping events are marked with asterisks. Conditions (substrate stiffness): 5 kPa (D, G, J, M); 15 kPa (physiological) (E, H, K, N); 85 kPa (F, I, L, O). (Figure 1.)

Haertter, Hauke, Driehorst et al 2026, eLife · CC BY 4.0

Lipid storage and metabolism are compromised in the hearts of the Pex11a knockout mice. ( A , B ): Electron micrographs of LDs (black arrowheads) and POs (black arrows) in LV cardiomyocytes of wild-type and knockout mice. ( C , D ): LD abundance ( C ) (calculated from "n" images as indicated in the graph) and size ( D ) (calculated from 233 LDs) derived from 3 mice/genotype. ( E , F ): IFA of PLIN2 in LVs. ( G ): Abundance of PLIN2-stained LDs in wild-type and knockout LVs calculated from 4 mice/genotype. (mouse (wild-type and Pex11a knockout left ventricular cardiomyocytes); Figure 5.)

Colasante, Chen, Garikapati et al 2025, Cells · CC BY 4.0

Structural organization of uninfected ex vivo ventricular cardiomyocytes at 6 weeks post-infection. The central panel shows a composite fluorescence microscopy image of cardiomyocytes stained with MitoTracker Green (mitochondria) and CellMask Deep Red (actin). Insets correspond to regions highlighted in transmission electron micrographs (TEM) from other samples. Mitochondria are loosely packed in the cardiomyocyte core, surrounded by a myofibril sheath, and may align parallel to adjacent actin myofibrils. (A) Mitochondria arranged between myofibrils (MF), oriented roughly parallel to the myofibrils. A circular void at the bottom likely represents a lipid droplet dislodged during ultra-fine sectioning. (B) A small fraction of mitochondria are positioned directly beneath the cell membrane (CM), labeled as subsarcolemmal mitochondria (SSM), with a visible nucleus (N). (C) Loosely packed mitochondria within the cardiomyocyte core, surrounded by a myofibril sheath. Mitochondria near the nucleus, identified as perinuclear mitochondria (PNM), while those further away are classified as intermyofibrillar mitochondria (IMFM), both indicated by arrows. The dotted line demarcates an arbitrary boundary between the PNM and IMFM regions. (D) A fraction of mitochondria within the myofibril sheath showing mammalian-like orientation, with tight contact between mitochondria and myofibrils. All TEM images were acquired from resin-embedded, stained 70 nm sections. Scale bars: 1000 nm (A-C) and 500 nm (D). (Atlantic salmon (ex vivo ventricular cardiomyocytes isolated from Salmo salar at 6 weeks post-infection); Figure 5.)

Malachowski, Wolfson, Olsen et al 2026, iScience · CC BY 4.0

Histopathological findings from endomyocardial biopsy of a heart transplant recipient (control). Sections stained with Masson's trichrome (A, D) revealed normal myocardial architecture without fibrosis, vacuolization, or inflammation, and normal density of mitochondria. A few patients exhibited inflammatory infiltrates (arrows) (B) and some small areas with vacuolization (C, D). Despite the presence of the latter, transmission electron micrographs do not reveal any glycogen deposits (E, F). TEM panels (D, E) show mitochondria (Mt), myofibrils (Mf), and sarcomere structure in normal human cardiomyocytes. (human (endomyocardial biopsy, heart transplant recipient control); Figure 2, full figure (control endomyocardial biopsy).)

Honorato-Sampaio et al. 2026, Arquivos Brasileiros de Cardiologia · CC BY 4.0

Immunofluorescence of iPSC-derived cardiomyocytes (iCMs) from a patient with Pompe disease (PD), showing cardiac hypertrophy phenotype. Cardiomyocytes are labeled with sarcomeric alpha-actinin (red) marking the sarcomere Z-discs and cardiac troponin T (cTnT, green) marking the thin filaments. DAPI (blue) labels nuclei. The iCMs show enlarged cell size and organized sarcomeric structure characteristic of cardiomyocyte differentiation. (human (iPSC-derived cardiomyocytes, Pompe disease patient); Figure 3, A-B.)

Huang W et al. 2024, Cell proliferation · CC BY 4.0

Papers

  1. Wang J, Zhu X, Li Y, Dai L, Tan X, Li J, et al. Patient-Derived iPSC-Cardiomyocytes Reveal Subclinical Cardiomyocyte Dysfunction Associated With the CAV3 N-Terminal Variant p.Ala46Thr. Hum Mutat. 2026;2026:4061668. PMID: 42774892.
  2. Haertter D, Hauke L, Driehorst T, Nishi K, Zimmermann WH, Schmidt CF. Sarcomere dynamic instability and stochastic heterogeneity drive robust cardiomyocyte contraction. Elife. 2026;13:RP97321. PMID: 42734122.
  3. Piavchenko G, Venediktov A, Shamitko Z, Urazova K, Obelchakova M, Khabarova E, et al. Polarized Light Microscopy for Quantitative Assessment of Sarcomere-Scale Structural Order in Cardiac Tissue. J Biophotonics. 2026;19:e70338. PMID: 42575126.
  4. Gaballah M, Penttinen K, Prajapati C, Aalto-Setälä K. Metabolic fatty acid substrates enhance the structural and mechanical performance of human-induced pluripotent stem cell-derived cardiomyocytes. Cell Mol Life Sci. 2026;83:297. PMID: 42565878.
  5. Malachowski A, Wolfson DL, Olsen R, Dalum AS, Opstad IS, Agarwal K, et al. Mitochondrial dynamics and antiviral responses in Atlantic salmon cardiomyocytes during piscine myocarditis virus infection. iScience. 2026;29:116831. PMID: 42495550.
  6. Jang Y, Shani K, Clouvel-Gervaiseau A, Prondzynski M, Nuebling S, Shin CJ, et al. Structural and functional benchmarking of monolayer- and bioreactor-generated hiPSC-derived cardiomyocytes. APL Bioeng. 2026;10:036102. PMID: 42428810.
  7. Ignatyeva N, Cheruiyot C, Saleem HN, Wali R, Plota D, Zhang W, et al. Targeting intracellular cholesterol imbalance rescues sarcomere-ER contact site signaling and ER remodeling in dilated cardiomyopathy. Signal Transduct Target Ther. 2026;11:237. PMID: 42303996.
  8. Honorato-Sampaio K, Oliveira C, Araújo SA, Correa FS, Dias GM, Bahia Neto AFC, et al. PRKAG2 Cardiomyopathy: A Case-Control Study on the Diagnostic Yield Of Histopathology and Ultrastructural Analysis from Endomyocardial Biopsy. Arq Bras Cardiol. 2026;123:e20240616. PMID: 41849454.
  9. Dutta PK, Toth JM, Sundaram S, Chen X, Chopra A, Ewoldt JK, et al. Cell shape and maturation impacts α-actinin-2 tension in iPSC-derived cardiomyocytes. APL Bioeng. 2026;10:016109. PMID: 41695113.
  10. Colasante C, Chen J, Garikapati V, Spengler B, Schlüter KD, Baumgart-Vogt E. The Knockout of PEX11a Results in Mild Peroxisomal Dysfunction and Lowered Cardiac Recovery Following Langendorff-Mediated Ischemia-Reperfusion in Mice. Cells. 2025;15:12. PMID: 41511296.
  11. Huang W, Zhou R, Jiang C, Wang J, Zhou Y, Xu X, et al. Mitochondrial dysfunction is associated with hypertrophic cardiomyopathy in Pompe disease-specific induced pluripotent stem cell-derived cardiomyocytes. Cell Prolif. 2024;57:e13573. PMID: 37916452.

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