This is a correction to Krstevski, C., Cohen, C.D., Dona, M.S.I. and Pinto, A.R. (2020) New perspectives of the cardiac cellular landscape: mapping cellular mediators of cardiac fibrosis using single-cell transcriptomics. Biochem. Soc. Trans.48, 2483–2493. 10.1042/BST20191255

Following publication of the above article, the authors noticed a citation was missing from the revised article resulting in errors in Table 1, where the reference numbers associated with studies summarised in the table are incorrect.

Table 1.
Single-cell transcriptomic studies investigating cellular and molecular drivers of cardiac fibrosis in heart failure
ContextReferenceCellsMean Reads/cellTechnologyNotes and key findings
Mouse myocardial infarction (101) 426 16,874 Sort-Seq • 3-days post-MI and sham control mice
• n = 3/group.
• Ckap4 proposed as a novel driver of myofibroblast differentiation. 
Mouse myocardial infarction (62) 13,331 ∼35,000 10X Chromium • 3- and 7-days post-MI and sham control.
• n=1/time point/group.
• Identified heterogeneous fibroblast and myofibroblast subsets involved in fibrosis. 
Mouse hypertension (Angiotensin II infusion) (56) 29,615 ∼80,000 10X Chromium • 2 weeks AngII-induced experimental   hypertension and control mice.
• n=4/sex/group.
• Novel fibroblasts Fibro-Cilp and   Fibro-Thbs4 implicated in AngII-induced   fibrosis.
• Almost all cardiac cell types contribute to   ECM remodeling after AngII treatment.
• Extensive cell and sex-specific gene   expression patterns in the non-stressed   and stressed hearts. 
Mouse myocardial infarction (66) 36,874 ∼46,000 10X Chromium • 1, 3, 5, 7, 14- and 28-days post-MI and   sham control.
• n= ∼3/group.
• Identified heterogeneous fibroblast and   myofibroblast subsets involved in fibrosis.
• Early differentiation of myofibroblasts are   associated with cardiac rupture. 
Healthy and heart failure human patients (100) 21,422 ∼300,000 (Median reads/cell) iCell8 • Healthy organ donors and patients with   HF.
• n=14 healthy controls, 8 HF patients.
• Endothelial cells and fibroblasts are key   players in cellular crosstalk in progression   of HF. 
ContextReferenceCellsMean Reads/cellTechnologyNotes and key findings
Mouse myocardial infarction (101) 426 16,874 Sort-Seq • 3-days post-MI and sham control mice
• n = 3/group.
• Ckap4 proposed as a novel driver of myofibroblast differentiation. 
Mouse myocardial infarction (62) 13,331 ∼35,000 10X Chromium • 3- and 7-days post-MI and sham control.
• n=1/time point/group.
• Identified heterogeneous fibroblast and myofibroblast subsets involved in fibrosis. 
Mouse hypertension (Angiotensin II infusion) (56) 29,615 ∼80,000 10X Chromium • 2 weeks AngII-induced experimental   hypertension and control mice.
• n=4/sex/group.
• Novel fibroblasts Fibro-Cilp and   Fibro-Thbs4 implicated in AngII-induced   fibrosis.
• Almost all cardiac cell types contribute to   ECM remodeling after AngII treatment.
• Extensive cell and sex-specific gene   expression patterns in the non-stressed   and stressed hearts. 
Mouse myocardial infarction (66) 36,874 ∼46,000 10X Chromium • 1, 3, 5, 7, 14- and 28-days post-MI and   sham control.
• n= ∼3/group.
• Identified heterogeneous fibroblast and   myofibroblast subsets involved in fibrosis.
• Early differentiation of myofibroblasts are   associated with cardiac rupture. 
Healthy and heart failure human patients (100) 21,422 ∼300,000 (Median reads/cell) iCell8 • Healthy organ donors and patients with   HF.
• n=14 healthy controls, 8 HF patients.
• Endothelial cells and fibroblasts are key   players in cellular crosstalk in progression   of HF. 

The authors apologise for the error and would like to correct the record by including a citation to the following paper as no. 101:

  Gladka MM, Molenaar B, de Ruiter H, van der Elst S, Tsui H, Versteeg D, et al. Single-Cell Sequencing of the Healthy and Diseased Heart Reveals Cytoskeleton-Associated Protein 4 as a New Modulator of Fibroblasts Activation. Circulation. 2018 Jul 10;138(2):166–180.

And updating the reader to the corrected table below: