IMR Press / RCM / Volume 24 / Issue 2 / DOI: 10.31083/j.rcm2402052
Open Access Review
The Molecular Mechanism and Therapeutic Strategy of Cardiorenal Syndrome Type 3
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1 Department of Nephrology, The Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing, Chongqing Clinical Research Center of Kidney and Urology Diseases, Xinqiao Hospital, Army Medical University (Third Military Medical University), 400037 Chongqing, China
2 Medical Division, Xinqiao Hospital, Army Medical University, 400037 Chongqing, China
3 Department of Oncology, Southwest Cancer Center, Southwest Hospital, Army Medical University, 400038 Chongqing, China
*Correspondence: zhoujie_fl@163.com (Jie Zhou); ikkyhuang@163.com (Yinghui Huang)
These authors contributed equally.
Rev. Cardiovasc. Med. 2023, 24(2), 52; https://doi.org/10.31083/j.rcm2402052
Submitted: 2 October 2022 | Revised: 17 November 2022 | Accepted: 22 November 2022 | Published: 6 February 2023
(This article belongs to the Special Issue Cardiorenal Syndrome in Acute Kidney Injury)
Copyright: © 2023 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.
Abstract

Cardiorenal syndrome type 3 (CRS3) is defined as acute kidney injury (AKI)-induced acute cardiac dysfunction, characterized by high morbidity and mortality. CRS3 often occurs in elderly patients with AKI who need intensive care. Approximately 70% of AKI patients develop into CRS3. CRS3 may also progress towards chronic kidney disease (CKD) and chronic cardiovascular disease (CVD). However, there is currently no effective treatment. Although the major intermediate factors that can mediate cardiac dysfunction remain elusive, recent studies have summarized the AKI biomarkers, identified direct mechanisms, including mitochondrial dysfunction, inflammation, oxidative stress, apoptosis and activation of the sympathetic nervous system (SNS) and renin-angiotensin-aldosterone system (RAAS), inflammasome, as well as indirect mechanisms such as fluid overload, electrolyte imbalances, acidemia and uremic toxins, which are involved in the pathophysiological changes of CRS3. This study reviews the main pathological characteristics, underlying molecular mechanisms, and potential therapeutic strategies of CRS3. Mitochondrial dysfunction and inflammatory factors have been identified as the key initiators and abnormal links between the impaired heart and kidney, which contribute to the formation of a vicious circle, ultimately accelerating the progression of CRS3. Therefore, targeting mitochondrial dysfunction, antioxidants, Klotho, melatonin, gene therapy, stem cells, exosomes, nanodrugs, intestinal microbiota and Traditional Chinese Medicine may serve as promising therapeutic approaches against CRS3.

Keywords
CRS3
mitochondrial dysfunction
crosstalk
molecular mechanisms
therapeutic strategies
Funding
82030023/Key program of the Natural Science Foundation of China
81800621/Natural Science Foundation of China
81802783/Natural Science Foundation of China
81873605/Natural Science Foundation of China
82170705/Natural Science Foundation of China
cstc2021ycjh-bgzxm0145/Chongqing Science and Technology Talent Program
cstc2021jcyj-msxmX0672/Natural Science Foundation of Chongqing Science & Technology Commission
CSTB2022NSCQMSX0220/Natural Science Foundation of Chongqing Science & Technology Commission
2018YQYLY004/Frontier specific projects of Xinqiao Hospital
2018XLC1007/Personal training Program for Clinical Medicine Research of Army Medical University
Figures
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