The DOI matches its Crossref record; 166 of the 166 references it cites were found in a registry or an index.
Obesity, kidney dysfunction, and inflammation: interactions in hypertension
Open accessAbstract
Obesity contributes 65–75% of the risk for human primary (essential) hypertension (HT) which is a major driver of cardiovascular and kidney diseases. Kidney dysfunction, associated with increased renal sodium reabsorption and compensatory glomerular hyperfiltration, plays a key role in initiating obesity-HT and target organ injury. Mediators of kidney dysfunction and increased blood pressure include (i) elevated renal sympathetic nerve activity (RSNA); (ii) increased antinatriuretic hormones such as angiotensin II and aldosterone; (iii) relative deficiency of natriuretic hormones; (iv) renal compression by fat in and around the kidneys; and (v) activation of innate and adaptive immune cells that invade tissues throughout the body, producing inflammatory cytokines/chemokines that contribute to vascular and target organ injury, and exacerbate HT. These neurohormonal, renal, and inflammatory mechanisms of obesity-HT are interdependent. For example, excess adiposity increases the adipocyte-derived cytokine leptin which increases RSNA by stimulating the central nervous system proopiomelanocortin-melanocortin 4 receptor pathway. Excess visceral, perirenal and renal sinus fat compress the kidneys which, along with increased RSNA, contribute to renin–angiotensin–aldosterone system activation, although obesity may also activate mineralocorticoid receptors independent of aldosterone. Prolonged obesity, HT, metabolic abnormalities, and inflammation cause progressive renal injury, making HT more resistant to therapy and often requiring multiple antihypertensive drugs and concurrent treatment of dyslipidaemia, insulin resistance, diabetes, and inflammation. More effective anti-obesity drugs are needed to prevent the cascade of cardiorenal, metabolic, and immune disorders that threaten to overwhelm health care systems as obesity prevalence continues to increase.
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Cites
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Cited by
Neeland, I. J., Lim, S., Tchernof, A., Gastaldelli, A., Rangaswami, J., Ndumele, C. E., Powell-Wiley, T. M., & Després, J.-P. (2024) · Nature Reviews Disease Primers · doi:10.1038/s41572-024-00563-5 · Cited by 463
Obesity and chronic kidney disease
Jiang, Z., Wang, Y., Zhao, X., Cui, H., Han, M., Ren, X., Gang, X., & Wang, G. (2023) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00179.2022 · Cited by 267
Hammoud, S. H., AlZaim, I., Al-Dhaheri, Y., Eid, A. H., & El-Yazbi, A. F. (2021) · Frontiers in Endocrinology · doi:10.3389/fendo.2021.707126 · Cited by 87
Packer, M., Zile, M. R., Kramer, C. M., Murakami, M., Ou, Y., & Borlaug, B. A. (2025) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2025.03.009 · Cited by 49
Metadata
- Authors
- Hall, J. E., Mouton, A. J., da Silva, A. A., Omoto, A. C. M., Wang, Z., Li, X., & do Carmo, J. M.
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2020-12-01
- Volume
- 117
- Issue
- 8
- Pages
- 1859-1876
- ISSN
- 0008-6363 (ISSN-L)
- 1755-3245
- OpenAlex
- W3107928135
- Cited by
- 265
- References
- 166
- FWCI
- 11.73
- Type
- journal article
- Language
- en
- Open access
- green
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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