Telmisartan

Telmisartan, an angiotensin II receptor blocker, was evaluated for its ability to protect against TNF‑α‑induced cartilage degradation in osteoarthritis. In human C28/I2 chondrocytes, telmisartan reduced TNF‑α‑driven oxidative stress by lowering mitochondrial reactive oxygen species and protein carbonyl production. It also inhibited the proinflammatory mediators IL‑1β, IL‑6, and MCP‑1. Most importantly, telmisartan reversed the TNF‑α‑induced decline in type II collagen mRNA and protein by upregulating the transcription factor SOX‑9; silencing SOX‑9 abolished this protection. The authors propose telmisartan as a promising osteoarthritis therapy that preserves cartilage extracellular matrix via SOX‑9 upregulation.

Fig. 1 Telmisartan alleviated TNF-α-induced expression of inflammatory factors human C28/I2 chondrocytes. (Zhang X, et al., 2021)

Telmisartan, an angiotensin II receptor blocker, was tested for its ability to prevent high‑fat diet‑induced neurovascular dysfunction in mice. After 16 weeks, diet‑induced obese mice showed a 30% reduction in neurovascular coupling response to whisker pad stimulation compared to lean controls. Telmisartan co‑treatment increased the response by 10% relative to untreated obese mice. Telmisartan also normalized diet‑induced reductions in cerebral blood flow and prevented anxiety‑like behavior, and it affected cellular senescence and string vessel formation. The authors conclude that telmisartan protects against neurovascular unit impairments in obesity and may help prevent obesity‑related cognitive deficits.

Fig. 2 TEL prevents neurovascular impairment upon HFD. (Huber G, et al., 2021)