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Chronic kidney disease activates the HDAC6-inflammatory axis in the heart and contributes to myocardial remodeling in mice: inhibition of HDAC6 alleviates chronic kidney disease-induced myocardial remodeling

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Chronic kidney disease (CKD) adversely affects the heart. The underlying mechanism and the interplay between the kidney and the heart are still obscure. We examined the cardiac effect using the unilateral ureteral obstruction (UUO)-induced CKD pre-clinical model in mice. Echocardiography, histopathology of the heart, myocardial mRNA expression of ANP and BNP, the extent of fibrotic (TGF-β, α-SMA, and collagen I) and epigenetic (histone deacetylases, namely HDAC3, HDAC4, and HDAC6) proteins, and myocardial inflammatory response were assessed. Six weeks of post-UUO surgery, we observed a compromised left-ventricular wall thickness and signs of cardiac hypertrophy, accumulation of fibrosis associated, and inflammatory proteins in the heart. In addition, we observed a perturbation of epigenetic proteins, especially HDAC3, HDAC4, and HDAC6, in the heart. Pharmacological inhibition of HDAC6 using ricolinostat (RIC) lessened cardiac damage and improved left-ventricular wall thickness. The RIC treatment substantially restored the serum cardiac injury markers, namely creatine kinase-MB and lactate dehydrogenase (LDH) activities, ANP and BNP mRNA expression, and heart histological changes. The extent of myocardial fibrotic proteins, phospho-NF-κB (p65), and pro-inflammatory cytokines (TNF-α, IL-18, and IL-1β) were significantly decreased in the RIC treatment group. Further findings revealed the CKD-induced infiltration of CD3, CD8a, CD11c, and F4/80 positive inflammatory cells in the heart. Treatment with RIC substantially reduced the myocardial infiltration of these inflammatory cells. From these findings, we believe that CKD-induced myocardial HDAC6 perturbation has a deteriorative effect on the heart, and inhibition of HDAC6 can be a promising approach to alleviate CKD-induced myocardial remodeling.

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Data supporting this study are included within the article.



Atrial natriuretic peptide


Brain natriuretic peptide


Blood urea nitrogen


Chronic kidney disease


Creatine kinase-MB


Cardiorenal syndrome


Cardiovascular disease


Extracellular matrix


Ejection fraction


Enzyme-linked immunosorbent assay


End-stage renal disease


Fractional shortening

H & E:

Hematoxylin and eosin stain


Histone deacetylases




Lactate dehydrogenase


Left-ventricular end-diastolic anterior wall thickness


Left-ventricular end-systolic anterior wall thickness


Left-ventricular hypertrophy


Left-ventricular end-diastolic posterior wall thickness


Left-ventricular end-systolic posterior wall thickness


Masson’s trichrome stain

NF-κB (p65):

Nuclear factor-kappa B (p65)


Quantitative real-time polymerase chain reaction




Signal transducer and activator of transcription 3


Transforming growth factor-beta


Tumor necrosis factor-alpha


Unilateral ureteral obstruction




Wheat germ agglutinin stain


Alfa-smooth muscle actin


  1. Aldana-Masangkay GI, Sakamoto KM (2011) The role of HDAC6 in cancer. BioMed Res Int 2011:875824.

    Article  CAS  Google Scholar 

  2. Baek J-H (2019) The impact of versatile macrophage functions on acute kidney injury and its outcomes. Front Physiol 10:1016.

    Article  PubMed  PubMed Central  Google Scholar 

  3. Berl T, Henrich W (2006) Kidney-heart interactions: epidemiology, pathogenesis, and treatment. Clin J Am Soc Nephrol 1:8–18.

    Article  CAS  PubMed  Google Scholar 

  4. Bhargava P, Schnellmann RG (2017) Mitochondrial energetics in the kidney. Nat Rev Nephrol 13:629–646.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  5. Cao Q, Wang Y, Wang XM, Lu J, Lee VW, Ye Q, Nguyen H, Zheng G, Zhao Y, Alexander SI, Harris DCH (2015) Renal F4/80+ CD11c+ mononuclear phagocytes display phenotypic and functional characteristics of macrophages in health and in adriamycin nephropathy. J Am Soc Nephrol: JASN 26:349.

    Article  CAS  PubMed  Google Scholar 

  6. Chen X, Yu C, Hou X, Li J, Li T, Qiu A, Liu N, Zhuang S (2020) Histone deacetylase 6 inhibition mitigates renal fibrosis by suppressing TGF-β and EGFR signaling pathways in obstructive nephropathy. Am J Physiol Renal Physiol 319:F1003–F1014.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  7. Cho E, Kim M, Ko YS, Lee HY, Song M, Kim MG, Kim H-K, Cho W-Y, Jo S-K (2013) Role of inflammation in the pathogenesis of cardiorenal syndrome in a rat myocardial infarction model. Nephrol Dial Transplant 28:2766–2778.

    Article  CAS  PubMed  Google Scholar 

  8. Chung AW, Sieling PA, Schenk M, Teles RM, Krutzik SR, Hsu DK, Liu F-T, Sarno EN, Rea TH, Stenger S, Modlin RL, Lee DJ (2013) Galectin-3 regulates the innate immune response of human monocytes. J Infect Dis 207:947–956.

    Article  CAS  PubMed  Google Scholar 

  9. Clementi A, Virzì GM, Battaglia GG, Ronco C (2019) Neurohormonal, endocrine, and immune dysregulation and inflammation in cardiorenal syndrome. Cardiorenal Med 9:265–273.

    Article  CAS  PubMed  Google Scholar 

  10. Costanzo MR (2022) The cardiorenal syndrome in heart failure. Cardiol Clin 40:219–235.

    Article  PubMed  Google Scholar 

  11. Demos-Davies KM, Ferguson BS, Cavasin MA, Mahaffey JH, Williams SM, Spiltoir JI, Schuetze KB, Horn TR, Chen B, Ferrara C, Scellini B, Piroddi N, Tesi C, Poggesi C, Jeong MY, McKinsey TA (2014) HDAC6 contributes to pathological responses of heart and skeletal muscle to chronic angiotensin-II signaling. Am J Physiol Heart Circ Physiol 307:H252–H258.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  12. Di Lullo L, Bellasi A, Barbera V, Russo D, Russo L, Di Iorio B, Cozzolino M, Ronco C (2017) Pathophysiology of the cardio-renal syndromes types 1–5: an uptodate. Indian Heart J 69:255–265.

    Article  PubMed  PubMed Central  Google Scholar 

  13. Dikow R, Adamczak M, Henriquez DE, Ritz E (2002) Strategies to decrease cardiovascular mortality in patients with end-stage renal disease. Kidney Int 61:S5–S10.

    Article  Google Scholar 

  14. Duffield JS (2010) Macrophages and immunologic inflammation of the kidney. Semin Nephrol 30:234–254.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  15. Epelman S, Lavine KJ, Beaudin AE, Sojka DK, Carrero JA, Calderon B, Brija T, Gautier EL, Ivanov S, Satpathy AT, Schilling JD, Schwendener R, Sergin I, Razani B, Forsberg EC, Yokoyama WM, Unanue ER, Colonna M, Randolph GJ, Mann DL (2014) Embryonic and adult-derived resident cardiac macrophages are maintained through distinct mechanisms at steady state and during inflammation. Immunity 40:91–104.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  16. Gairola S, Ram C, Syed AM, Doye P, Kulhari U, Mugale MN, Murty US, Sahu BD (2021) Nootkatone confers antifibrotic effect by regulating the TGF-β/Smad signaling pathway in mouse model of unilateral ureteral obstruction. Eur J Pharmacol 910:174479.

    Article  CAS  PubMed  Google Scholar 

  17. Gajjala PR, Sanati M, Jankowski J (2015) Cellular and molecular mechanisms of chronic kidney disease with diabetes mellitus and cardiovascular diseases as its comorbidities. Front Immunol 6:340.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  18. Ham O, Jin W, Lei L, Huang HH, Tsuji K, Huang M, Roh J, Rosenzweig A, Lu HAJ (2018) Pathological cardiac remodeling occurs early in CKD mice from unilateral urinary obstruction, and is attenuated by Enalapril. Sci Rep 8:16087.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  19. Heidt T, Courties G, Dutta P, Sager HB, Sebas M, Iwamoto Y, Sun Y, Da Silva N, Panizzi P, van der Laan AM, Swirski FK, Weissleder R, Nahrendorf M (2014) Differential contribution of monocytes to heart macrophages in steady-state and after myocardial infarction. Circ Res 115:284–295.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  20. Henderson NC, Mackinnon AC, Farnworth SL, Kipari T, Haslett C, Iredale JP, Liu F-T, Hughes J, Sethi T (2008) Galectin-3 expression and secretion links macrophages to the promotion of renal fibrosis. Am J Pathol 172:288–298.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  21. Herzog CA, Asinger RW, Berger AK, Charytan DM, Díez J, Hart RG, Eckardt K-U, Kasiske BL, McCullough PA, Passman RS, DeLoach SS, Pun PH, Ritz E (2011) Cardiovascular disease in chronic kidney disease. A clinical update from kidney disease: improving global outcomes (KDIGO). Kidney Int 80:572–586.

    Article  PubMed  Google Scholar 

  22. Hewitson TD, Holt SG, Smith ER (2015) Animal models to study links between cardiovascular disease and renal failure and their relevance to human pathology. Front Immunol 6:465.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  23. Hof A, Geißen S, Singgih K, Mollenhauer M, Winkels H, Benzing T, Baldus S, Hoyer FF (2022) Myeloid leukocytes’ diverse effects on cardiovascular and systemic inflammation in chronic kidney disease. Basic Res Cardiol 117:38.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  24. Hulsmans M, Sager HB, Roh JD, Valero-Muñoz M, Houstis NE, Iwamoto Y, Sun Y, Wilson RM, Wojtkiewicz G, Tricot B, Osborne MT, Hung J, Vinegoni C, Naxerova K, Sosnovik DE, Zile MR, Bradshaw AD, Liao R, Tawakol A, Weissleder R, Rosenzweig A, Swirski FK, Sam F, Nahrendorf M (2018) Cardiac macrophages promote diastolic dysfunction. J Exp Med 215:423–440.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  25. Kee HJ, Bae EH, Park S, Lee KE, Suh SH, Kim SW, Jeong MH (2013) HDAC inhibition suppresses cardiac hypertrophy and fibrosis in DOCA-salt hypertensive rats via regulation of HDAC6/HDAC8 enzyme activity. Kidney Blood Press Res 37:229–239.

    Article  CAS  PubMed  Google Scholar 

  26. Laroumanie F, Douin-Echinard V, Pozzo J, Lairez O, Tortosa F, Vinel C, Delage C, Calise D, Dutaur M, Parini A, Pizzinat N (2014) CD4+ T cells promote the transition from hypertrophy to heart failure during chronic pressure overload. Circulation 129:2111–2124.

    Article  CAS  PubMed  Google Scholar 

  27. Lemon DD, Horn TR, Cavasin MA, Jeong MY, Haubold KW, Long CS, Irwin DC, McCune SA, Chung E, Leinwand LA, McKinsey TA (2011) Cardiac HDAC6 catalytic activity is induced in response to chronic hypertension. J Mol Cell Cardiol 51:41–50.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  28. Leucker TM, Nomura Y, Kim JH, Bhatta A, Wang V, Wecker A, Jandu S, Santhanam L, Berkowitz D, Romer L, Pandey D (2017) Cystathionine γ-lyase protects vascular endothelium: a role for inhibition of histone deacetylase 6. Am J Physiol Heart Circ Physiol 312:H711–H720.

    Article  PubMed  PubMed Central  Google Scholar 

  29. Li L, Liu F, Huang W, Wang J, Wan Y, Li M, Pang Y, Yin Z (2019) Ricolinostat (ACY-1215) inhibits VEGF expression via PI3K/AKT pathway and promotes apoptosis in osteoarthritic osteoblasts. Biomed Pharmacother 118:109357.

    Article  CAS  PubMed  Google Scholar 

  30. Liu H (2021) The roles of histone deacetylases in kidney development and disease. Clin Exp Nephrol 25:215–223.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  31. Liu M, Li X-C, Lu L, Cao Y, Sun R-R, Chen S, Zhang P-Y (2014) Cardiovascular disease and its relationship with chronic kidney disease. Eur Rev Med Pharmacol Sci 18:2918–2926 (PMID: 25339487)

    CAS  PubMed  Google Scholar 

  32. Liu N, Zhuang S (2015) Treatment of chronic kidney diseases with histone deacetylase inhibitors. Front Physiol 6:121.

    Article  PubMed  PubMed Central  Google Scholar 

  33. Liu S (2019) Heart-kidney interactions: mechanistic insights from animal models. Am J Physiol Renal Physiol 316:F974–F985.

    Article  CAS  PubMed  Google Scholar 

  34. LoPresti P (2020) HDAC6 in diseases of cognition and of neurons. Cells 10:12.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  35. Mall G, Huther W, Schneider J, Lundin P, Ritz E (1990) Diffuse intermyocardiocytic fibrosis in uraemic patients. Nephrol Dial Transplant 5:39–44.

    Article  CAS  PubMed  Google Scholar 

  36. Mall G, Rambausek M, Neumeister A, Kollmar S, Vetterlein F, Ritz E (1988) Myocardial interstitial fibrosis in experimental uremia—implications for cardiac compliance. Kidney Int 33:804–811.

    Article  CAS  PubMed  Google Scholar 

  37. Manalo T, May A, Quinn J, Lafontant DS, Shifatu O, He W, Gonzalez-Rosa JM, Burns GC, Burns CE, Burns AR, Lafontant PJ (2016) Differential lectin binding patterns identify distinct heart regions in giant danio (Devario aequipinnatus) and zebrafish (Danio rerio) hearts. J Histochem Cytochem 64:687–714.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  38. Martina MN, Bandapalle S, Rabb H, Hamad AR (2014) Isolation of double negative αβ T cells from the kidney. JoVE J Vis Exp.

    Article  PubMed  Google Scholar 

  39. Martínez-Klimova E, Aparicio-Trejo OE, Tapia E, Pedraza-Chaverri J (2019) Unilateral ureteral obstruction as a model to investigate fibrosis-attenuating treatments. Biomolecules 9:141.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  40. Matsushita K, Saritas T, Eiwaz MB, McClellan N, Coe I, Zhu W, Ferdaus MZ, Sakai LY, McCormick JA, Hutchens MP (2020) The acute kidney injury to chronic kidney disease transition in a mouse model of acute cardiorenal syndrome emphasizes the role of inflammation. Kidney Int 97:95–105.

    Article  CAS  PubMed  Google Scholar 

  41. Mawhin M, Bright R, Fourre J, Vloumidi E, Tomlinson J, Sardini A, Pusey C, Woollard K (2022) Chronic kidney disease mediates cardiac dysfunction associated with increased resident cardiac macrophages. BMC Nephrol 23:47.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  42. Nevers T, Salvador AM, Grodecki-Pena A, Knapp A, Velázquez F, Aronovitz M, Kapur NK, Karas RH, Blanton RM, Alcaide P (2015) Left ventricular T-cell recruitment contributes to the pathogenesis of heart failure. Circ Heart Fail 8:776–787.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  43. Nie J, Duan Q, He M, Li X, Wang B, Zhou C, Wu L, Wen Z, Chen C, Wang DW, Alsina KM, Wehrens XH-T, Wang DW, Ni L (2019) Ranolazine prevents pressure overload-induced cardiac hypertrophy and heart failure by restoring aberrant Na+ and Ca2+ handling. J Cell Physiol 234:11587–11601.

    Article  CAS  PubMed  Google Scholar 

  44. Nie L, Liu Y, Zhang B, Zhao J (2020) Application of histone deacetylase inhibitors in renal interstitial fibrosis. Kidney Dis 6:226–235.

    Article  Google Scholar 

  45. Pang M, Zhuang S (2010) Histone deacetylase: a potential therapeutic target for fibrotic disorders. J Pharmacol Exp Ther 335:266–272.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  46. Pereira BJ, Shapiro L, King AJ, Falagas ME, Strom JA, Dinarello CA (1994) Plasma levels of IL-1β, TNFα and their specific inhibitors in undialyzed chronic renal failure, CAPD and hemodialysis patients. Kidney Int 45:890–896.

    Article  CAS  PubMed  Google Scholar 

  47. Radeke HH, Meier B, Topley N, Flöge J, Habermehl GG, Resch K (1990) Interleukin 1-α and tumor necrosis factor-α induce oxygen radical production in mesangial cells. Kidney Int 37:767–775.

    Article  CAS  PubMed  Google Scholar 

  48. Rosner MH, Ronco C, Okusa MD (2012) The role of inflammation in the cardio-renal syndrome: a focus on cytokines and inflammatory mediators. Semin Nephrol 32:70–78.

    Article  CAS  PubMed  Google Scholar 

  49. Sachdeva J, Dai W, Kloner RA (2014) Functional and histological assessment of an experimental model of Takotsubo’s cardiomyopathy. J Am Heart Assoc 3:e000921.

    Article  PubMed  PubMed Central  Google Scholar 

  50. Sahu BD, Kumar JM, Sistla R (2015) Baicalein, a bioflavonoid, prevents cisplatin-induced acute kidney injury by up-regulating antioxidant defenses and down-regulating the MAPKs and NF-κB pathways. PLoS ONE 10:e0134139.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  51. Song R, Yang Y, Lei H, Wang G, Huang Y, Xue W, Wang Y, Yao L, Zhu Y (2018) HDAC6 inhibition protects cardiomyocytes against doxorubicin-induced acute damage by improving α-tubulin acetylation. J Mol Cell Cardiol 124:58–69.

    Article  CAS  PubMed  Google Scholar 

  52. Soppert J, Frisch J, Wirth J, Hemmers C, Boor P, Kramann R, Vondenhoff S, Moellmann J, Lehrke M, Hohl M, Vorst EP-CVD, Werner C, Speer T, Maack C, Marx N, Jankowski J, Roma LP, Noels H (2022) A systematic review and meta-analysis of murine models of uremic cardiomyopathy. Kidney Int 101:256–273.

    Article  CAS  PubMed  Google Scholar 

  53. Stenvinkel P, Ketteler M, Johnson RJ, Lindholm B, Pecoits-Filho R, Riella M, Heimbürger O, Cederholm T, Girndt M (2005) IL-10, IL-6, and TNF-α: central factors in the altered cytokine network of uremia-the good, the bad, and the ugly. Kidney Int 67:1216–1233.

    Article  CAS  PubMed  Google Scholar 

  54. Taddei S, Nami R, Bruno RM, Quatrini I, Nuti R (2011) Hypertension, left ventricular hypertrophy and chronic kidney disease. Heart Fail Rev 16:615–620.

    Article  PubMed  Google Scholar 

  55. Tyralla K, Amann K (2002) Cardiovascular changes in renal failure. Blood Purif 20:462–465.

    Article  PubMed  Google Scholar 

  56. Virzì GM, Day S, de Cal M, Vescovo G, Ronco C (2014) Heart–kidney crosstalk and role of humoral signaling in critical illness. Crit Care 18:1–11.

    Article  Google Scholar 

  57. Virzì GM, Torregrossa R, Cruz DN, Chionh CY, De Cal M, Soni SS, Dominici M, Vescovo G, Rosner MH, Ronco C (2012) Cardiorenal syndrome type 1 may be immunologically mediated: a pilot evaluation of monocyte apoptosis. Cardiorenal Med 2:33–42.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  58. Virzì GM, Zhang J, Nalesso F, Ronco C, McCullough PA (2018) The role of dendritic and endothelial cells in cardiorenal syndrome. Cardiorenal Med 8:92–104.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  59. Wollenhaupt J, Frisch J, Harlacher E, Wong DW, Jin H, Schulte C, Vondenhoff S, Moellmann J, Klinkhammer BM, Zhang L, Baleanu-Curaj A, Liehn EA, Speer T, Kazakov A, Werner C, Vorst EP-CVD, Selejan SR, Hohl M, Böhm M, Kramann R, Biessen EA-L, Lehrke M, Marx N, Jankowski J, Maack C, Boor P, Roma LP, Noels H (2022) Pro-oxidative priming but maintained cardiac function in a broad spectrum of murine models of chronic kidney disease. Redox Biol 56:102459

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  60. Yang W-N, Hu X-D, Han H, Shi L-L, Feng G-F, Liu Y, Qian Y-H (2014) The effects of valsartan on cognitive deficits induced by aluminum trichloride and d-galactose in mice. Neurol Res 36:651–658.

    Article  CAS  PubMed  Google Scholar 

  61. Zhang D, Wu C-T, Qi X, Meijering RA, Hoogstra-Berends F, Tadevosyan A, Cubukcuoglu Deniz G, Durdu S, Akar AR, Sibon OC (2014) Activation of histone deacetylase-6 induces contractile dysfunction through derailment of α-tubulin proteostasis in experimental and human atrial fibrillation. Circulation 129:346–358.

    Article  CAS  PubMed  Google Scholar 

  62. Zhao Y, Wang C, Hong X, Miao J, Liao Y, Hou FF, Zhou L, Liu Y (2019) Wnt/β-catenin signaling mediates both heart and kidney injury in type 2 cardiorenal syndrome. Kidney Int 95:815–829.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  63. Zoccali C, Vanholder R, Massy ZA, Ortiz A, Sarafidis P, Dekker FW, Fliser D, Fouque D, Heine GH, Jager KJ, Kanbay M, Mallamaci F, Parati G, Rossignol P, Wiecek A, London G (2017) The systemic nature of CKD. Nat Rev Nephrol 13:344–358.

    Article  PubMed  Google Scholar 

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The study is supported by a Start-Up Research Grant in Life Sciences (Grant No. SRG/2021/000428) of the Science and Engineering Research Board (SERB), Department of Science and Technology (DST), Government of India, New Delhi.

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Authors and Affiliations



Sourav Kundu and Shobhit Gairola: conceptualization, methodology, formal analysis, investigation, writing—original draft. Smriti Verma and Madhav Nilakanth Mugale: methodology (histopathology studies), formal analysis, and investigation. Bidya Dhar Sahu: conceptualization, supervision, funding acquisition, and writing—review and editing.

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Correspondence to Bidya Dhar Sahu.

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The animal study protocol was reviewed and approved by the Institutional Animal Ethics Committee (IAEC) of the NIPER Guwahati (Approval No. NIPER/PC/2022/04) and performed in accordance with the Committee for Control and Supervision of Experiments on Animals (CCSEA), Government of India.

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Kundu, S., Gairola, S., Verma, S. et al. Chronic kidney disease activates the HDAC6-inflammatory axis in the heart and contributes to myocardial remodeling in mice: inhibition of HDAC6 alleviates chronic kidney disease-induced myocardial remodeling. Basic Res Cardiol (2024).

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